Updated on 2025/08/22

写真a

 
TAKAHASHI Motoko
 
Organization
School of Medicine Department of Biochemistry Professor
Title
Professor
Homepage
https://web.sapmed.ac.jp/biochem1/index.html
External link

Degree

  • 医学博士 ( 大阪大学 )

Research Interests

  • 糖鎖生物学 酸化還元酵素 タンパク質糖化反応

Research Areas

  • Life Science / Pathological biochemistry

  • Life Science / Medical biochemistry

Education

  • 大阪大学大学院   医学系研究科

    1991.4 - 1995.3

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    Country： Japan

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  • Hokkaido University   School of Medicine

    1985.4 - 1991.3

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    Country： Japan

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Research History

  • Sapporo Medical University School of Medicine   Department of Biochemistry   Professor

    2017.9

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  • Sapporo Medical University   School of Medicine, Department of Biochemistry   Associate Professor

    2007.1 - 2017.8

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  • Saga University   Faculty of Medicine   Associate Professor (as old post name)

    2005.1 - 2006.12

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  • Osaka University   Faculty of Medicine   Research Assistant

    1998.3 - 2004.12

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Professional Memberships

  • THE JAPANESE CANCER ASSOCIATION

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  • THE JAPANESE SOCIETY OF CARBOHYDRATE RESEARCH

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  • Japan Maillard Reaction Society

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  • SOCIETY FOR FREE RADICAL RESEARCH JAPAN

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  • THE JAPANESE BIOCHEMICAL SOCIETY

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Committee Memberships

  • 日本糖質学会   評議員  

       

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    Committee type：Academic society

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  • 日本生化学会   評議員  

       

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    Committee type：Academic society

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  • 日本メイラード学会   世話人  

       

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    Committee type：Academic society

    日本メイラード学会

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Papers

  • Site-specific glycosylation analysis of epidermal growth factor receptor 2 (ErbB2): exploring structure and function toward therapeutic targeting. International journal

    Naoki Fujitani, Yasuaki Uehara, Shigeru Ariki, Ukichiro Hashimoto, Jo Mukai, Yoshihiro Hasegawa, Motoko Takahashi

    Glycobiology   34 ( 3 )   2024.4

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    Language：English   Publishing type：Research paper (scientific journal)  

    Glycans found on receptor tyrosine kinases (RTKs) have emerged as promising targets for cancer chemotherapy, aiming to address issues such as drug resistance. However, to effectively select the target glycans, it is crucial to define the structure and function of candidate glycans in advance. Through mass spectrometric analysis, this study presents a "glycoform atlas" of epidermal growth factor receptor 2 (ErbB2), an RTK targeted for the treatment of ErbB2-positive cancers. Our analysis provides an in-depth and site-specific glycosylation profile, including both asparagine- and serine/threonine-linked glycosylation. Molecular dynamics simulations of N-glycosylated ErbB2 incorporating the identified glycan structures suggested that the N-glycan at N124 on the long flexible loop in the N-terminal region plays a role in stabilizing the ErbB2 structure. Based on the model structures obtained from the simulations, analysis employing an ErbB2 mutant deficient in N-glycosylation at N124 exhibited a significantly shorter intracellular half-life and suppressed autophosphorylation compared to wild-type ErbB2. Moreover, a structural comparison between the N-glycosylated forms of ErbB2 and its structurally homologous receptor, epidermal growth factor receptor (EGFR), demonstrated distinct variations in the distribution and density of N-glycans across these two molecules. These findings provide valuable insights into the structural and functional implications of ErbB2 glycosylation and will contribute to facilitating the establishment of glycan-targeted therapeutic strategies for ErbB2-positive cancers.

    DOI： 10.1093/glycob/cwad100

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  • N-glycan on N262 of FGFR3 regulates the intracellular localization and phosphorylation of the receptor. International journal

    Ukichiro Hashimoto, Naoki Fujitani, Yasuaki Uehara, Hiromi Okamoto, Atsushi Saitou, Fumie Ito, Shigeru Ariki, Akiko Shiratsuchi, Yoshihiro Hasegawa, Motoko Takahashi

    Biochimica et biophysica acta. General subjects   1868 ( 4 )   130565 - 130565   2024.4

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    Language：English   Publishing type：Research paper (scientific journal)  

    N-glycosylation and proper processing of N-glycans are required for the function of membrane proteins including cell surface receptors. Fibroblast growth factor receptor (FGFR) is involved in a wide variety of biological processes including embryonic development, osteogenesis, angiogenesis, and cell proliferation. Human FGFR3 contains six potential N-glycosylation sites, however, the roles of glycosylation have not been elucidated. The site-specific profiles of N-glycans of the FGFR3 extracellular domain expressed and secreted by CHO-K1 cells were examined, and glycan occupancies and structures of four sites were determined. The results indicated that most sites were fully occupied by glycans, and the dominant populations were the complex type. By examining single N-glycan deletion mutants of FGFR3, it was found that N262Q mutation significantly increased the population with oligomannose-type N-glycans, which was localized in the endoplasmic reticulum. Protein stability assay suggested that fraction with oligomannose-type N-glycans in the N262Q mutant is more stable than those in the wild type and other mutants. Furthermore, it was found that ligand-independent phosphorylation was significantly upregulated in N262Q mutants with complex type N-glycans. The findings suggest that N-glycans on N262 of FGFR3 affect the intracellular localization and phosphorylation status of the receptor.

    DOI： 10.1016/j.bbagen.2024.130565

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  • FGFR3のN型糖鎖は細胞膜への発現と活性を制御する

    橋本 宇吉郎, 藤谷 直樹, 上原 康昭, 長谷川 喜弘, 有木 茂, 高橋 素子

    日本生化学会大会プログラム・講演要旨集   96回   [1P - 009]   2023.10

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  • FGFR1のN型糖鎖はレセプターの細胞内輸送と自己リン酸化を制御する

    岡本 弘美, 藤谷 直樹, 上原 康昭, 長谷川 喜弘, 橋本 宇吉郎, 有木 茂, 白土 明子, 高橋 素子

    日本生化学会大会プログラム・講演要旨集   96回   [1P - 044]   2023.10

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  • RANK C175R変異はERストレスを誘導し大理石骨病を引き起こす

    上原 康昭, 藤谷 直樹, 長谷川 喜弘, 有木 茂, 橋本 宇吉郎, 高橋 素子

    日本生化学会大会プログラム・講演要旨集   96回   [1P - 137]   2023.10

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  • ErbB2(HER2)の分子安定性に関与するN-glycansの機能の評価

    藤谷 直樹, 上原 康昭, 長谷川 喜弘, 橋本 宇吉郎, 有木 茂, 高橋 素子

    日本生化学会大会プログラム・講演要旨集   96回   [1P - 008]   2023.10

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  • Site-specific Analysis of <i>N</i>-glycans of Receptor Tyrosine Kinases

    Motoko Takahashi, Naoki Fujitani, Yasuaki Uehara, Yoshihiro Hasegawa

    Trends in Glycoscience and Glycotechnology   35 ( 206 )   E56 - E60   2023.7

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    Publishing type：Research paper (scientific journal)   Publisher：Forum: Carbohydrates Coming of Age  

    DOI： 10.4052/tigg.2212.1e

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  • Tumor-infiltrating Leukocyte Profiling Defines Three Immune Subtypes of NSCLC with Distinct Signaling Pathways and Genetic Alterations Reviewed International journal

    Aoki, K, Nishito, Y, Motoi, N, Arai, Y, Hiraoka, N, Shibata, T, Sonobe, Y, Kayukawa, Y, Hashimoto, E, Takahashi, M, Fujii, E, Nishizawa, T, Fukuda, H, Ohashi, K, Arai, K, Mizoguchi, Y, Yoshida, Y, Watanabe, S, Yamashita, M, Kitano, S, Sakamoto, H, Nagata, A, Mitsumori, R, Ozaki, K, Niida, S, Kanai, Y, Hirayama, A, Soga, T, Maruyama, T, Tsukada, K, Yabuki, N, Shimada, M, Kitazawa, T, Natori, O, Sawada, N, Kato, A, Yoshida, T, Yasuda, K, Mizuno, H, Tsunoda, H, Ochiai, A

    Cancer Res. Commun.   3 ( 6 )   1026 - 1040   2023.6

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    Language：English   Publishing type：Research paper (scientific journal)  

    Resistance to immune checkpoint blockade remains challenging in patients with non-small cell lung cancer (NSCLC). Tumor-infiltrating leukocyte (TIL) quantity, composition, and activation status profoundly influence responsiveness to cancer immunotherapy. This study examined the immune landscape in the NSCLC tumor microenvironment by analyzing TIL profiles of 281 fresh resected NSCLC tissues. Unsupervised clustering based on numbers and percentages of 30 TIL types classified adenocarcinoma (LUAD) and squamous cell carcinoma (LUSQ) into the cold, myeloid cell-dominant, and CD8+ T cell-dominant subtypes. These were significantly correlated with patient prognosis; the myeloid cell subtype had worse outcomes than the others. Integrated genomic and transcriptomic analyses, including RNA sequencing, whole-exome sequencing, T-cell receptor repertoire, and metabolomics of tumor tissue, revealed that immune reaction-related signaling pathways were inactivated, while the glycolysis and K-ras signaling pathways activated in LUAD and LUSQ myeloid cell subtypes. Cases with ALK and ROS1 fusion genes were enriched in the LUAD myeloid subtype, and the frequency of TERT copy-number variations was higher in LUSQ myeloid subtype than in the others. These classifications of NSCLC based on TIL status may be useful for developing personalized immune therapies for NSCLC.

    Significance: The precise TIL profiling classified NSCLC into novel three immune subtypes that correlates with patient outcome, identifying subtype-specific molecular pathways and genomic alterations that should play important roles in constructing subtype-specific immune tumor microenvironments. These classifications of NSCLC based on TIL status are useful for developing personalized immune therapies for NSCLC.

    DOI： 10.1158/2767-9764.CRC-22-0415

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  • Junctional adhesion molecule 3 is a potential therapeutic target for small cell lung carcinoma. International journal

    Miki Yamaguchi, Sachie Hirai, Masashi Idogawa, Toshiyuki Sumi, Hiroaki Uchida, Naoki Fujitani, Motoko Takahashi, Yuji Sakuma

    Experimental cell research   426 ( 2 )   113570 - 113570   2023.5

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    There are few effective therapies for small cell lung carcinoma (SCLC); thus, we need to develop novel and efficacious treatments. We hypothesized that an antibody-drug conjugate (ADC) could be a promising option for SCLC. Several publicly available databases were used to demonstrate the extent to which junctional adhesion molecule 3 (JAM3) mRNA was expressed in SCLC and lung adenocarcinoma cell lines and tissues. Three SCLC cell lines, Lu-135, SBC-5, and Lu-134 A, were selected and examined for JAM3 protein expression by flow cytometry. Finally, we examined the response of the three SCLC cell lines to a conjugate between an anti-JAM3 monoclonal antibody HSL156 (developed in-house) and the recombinant protein DT3C, which consists of diphtheria toxin lacking the receptor-binding domain but containing the C1, C2, and C3 domains of streptococcal protein G. In silico analyses revealed that JAM3 mRNA was expressed higher in SCLC cell lines and tissues than in those of lung adenocarcinoma. As expected, all the three SCLC cell lines examined were positive for JAM3 at the mRNA and protein levels. Consequently, control SCLC cells, but not JAM3-silenced ones, were highly sensitive to HSL156-DT3C conjugates, resulting in dose- and time-dependent decreased viability. Finally, silencing JAM3 alone suppressed the growth of all SCLC cell lines examined. Taken together, these findings suggest that an ADC targeting JAM3 could represent a new approach to treating SCLC patients.

    DOI： 10.1016/j.yexcr.2023.113570

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  • Quality Control of Targeted Plasma Lipids in a Large-Scale Cohort Study Using Liquid Chromatography–Tandem Mass Spectrometry Reviewed International journal

    Hirayama, A, Ishikawa, T, Takahashi, H, Yamanaka, S, Ikeda, S, Hirata, A, Harada, S, Sugimoto, M, Soga, T, Tomita, M, Takebayashi, T

    Metabolites   13 ( 4 )   558 - 558   2023.4

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：MDPI AG  

    High-throughput metabolomics has enabled the development of large-scale cohort studies. Long-term studies require multiple batch-based measurements, which require sophisticated quality control (QC) to eliminate unexpected bias to obtain biologically meaningful quantified metabolomic profiles. Liquid chromatography–mass spectrometry was used to analyze 10,833 samples in 279 batch measurements. The quantified profile included 147 lipids including acylcarnitine, fatty acids, glucosylceramide, lactosylceramide, lysophosphatidic acid, and progesterone. Each batch included 40 samples, and 5 QC samples were measured for 10 samples of each. The quantified data from the QC samples were used to normalize the quantified profiles of the sample data. The intra- and inter-batch median coefficients of variation (CV) among the 147 lipids were 44.3% and 20.8%, respectively. After normalization, the CV values decreased by 42.0% and 14.7%, respectively. The effect of this normalization on the subsequent analyses was also evaluated. The demonstrated analyses will contribute to obtaining unbiased, quantified data for large-scale metabolomics.

    DOI： 10.3390/metabo13040558

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  • ヒトRANKの糖鎖による機能制御メカニズムの解析

    上原 康昭, 藤谷 直樹, 長谷川 喜弘, 有木 茂, 橋本 宇吉郎, 岡本 弘美, 高橋 素子

    日本生化学会大会プログラム・講演要旨集   95回   2P - 034   2022.11

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  • ヒトErbB2(HER2)の部位特異的糖鎖構造解析

    藤谷 直樹, 上原 康昭, 長谷川 喜弘, 橋本 宇吉郎, 有木 茂, 高橋 素子

    日本生化学会大会プログラム・講演要旨集   95回   3P - 006   2022.11

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  • FGFR1の糖鎖の部位特異的構造解析と機能解析

    岡本 弘美, 藤谷 直樹, 上原 康昭, 長谷川 喜弘, 橋本 宇吉郎, 有木 茂, 白土 明子, 高橋 素子

    日本生化学会大会プログラム・講演要旨集   95回   1T02a - 06   2022.11

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  • RANK C175R変異は細胞膜への輸送障害を引き起こしRANKLへの刺激応答を抑制する

    上原 康昭, 藤谷 直樹, 長谷川 喜弘, 有木 茂, 橋本 宇吉郎, 高橋 素子

    日本骨代謝学会学術集会プログラム抄録集   40回   125 - 125   2022.7

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  • 呼吸器病学の若手研究最前線 肺胞微石症における肺破骨細胞様細胞の機能解析

    上原 康昭, 長谷川 喜弘, 高橋 素子, McCormack Francis X.

    日本呼吸器学会誌   11 ( 増刊 )   44 - 44   2022.4

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  • N-glycosylation regulates MET processing and signaling. International journal

    Atsushi Saitou, Yoshihiro Hasegawa, Naoki Fujitani, Shigeru Ariki, Yasuaki Uehara, Ukichiro Hashimoto, Atsushi Saito, Koji Kuronuma, Kunio Matsumoto, Hirofumi Chiba, Motoko Takahashi

    Cancer science   113 ( 4 )   1292 - 1304   2022.4

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    MET, the receptor for the hepatocyte growth factor (HGF), is strongly associated with resistance to tyrosine kinase inhibitors, key drugs that are used in the therapy of non-small cell lung cancer. MET contains 11 potential N-glycosylation sites, but the site-specific roles of these N-glycans have not been elucidated. We report herein that these N-glycans regulate the proteolytic processing of MET and HGF-induced MET signaling, and that this regulation is site specific. Inhibitors of N-glycosylation were found to suppress the processing and trafficking of endogenous MET in H1975 and EBC-1 lung cancer cells and exogenous MET in CHO-K1 cells. We purified the recombinant extracellular domain of human MET and determined the site-specific N-glycan structures and occupancy using mass spectrometry. The results indicated that most sites were fully glycosylated and that the dominant population was the complex type. To examine the effects of the deletion of N-glycans of MET, we prepared endogenous MET knockout Flp-In CHO cells and transfected them with a series of N-glycan-deletion mutants of MET. The results showed that several N-glycans are implicated in the processing of MET. The findings also suggested that the N-glycans of the SEMA domain of MET positively regulate HGF signaling, and the N-glycans of the region other than the SEMA domain negatively regulate HGF signaling. Processing, cell surface expression, and signaling were significantly suppressed in the case of the all-N-glycan-deletion mutant. The overall findings suggest that N-glycans of MET affect the status and the function of the receptor in a site-specific manner.

    DOI： 10.1111/cas.15278

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  • Role of glycosyltransferases in carcinogenesis; growth factor signaling and EMT/MET programs. International journal

    Motoko Takahashi, Yoshihiro Hasegawa, Kento Maeda, Masato Kitano, Naoyuki Taniguchi

    Glycoconjugate journal   39 ( 2 )   167 - 176   2022.4

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    Language：English   Publishing type：Research paper (scientific journal)  

    The glycosylation of cell surface receptors has been shown to regulate each step of signal transduction, including receptor trafficking to the cell surface, ligand binding, dimerization, phosphorylation, and endocytosis. In this review we focus on the role of glycosyltransferases that are involved in the modification of N-glycans, such as the effect of branching and elongation in signaling by various cell surface receptors. In addition, the role of those enzymes in the EMT/MET programs, as related to differentiation and cancer development, progress and therapy resistance is discussed.

    DOI： 10.1007/s10719-022-10041-3

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  • 呼吸器病学の若手研究最前線 肺胞微石症における肺破骨細胞様細胞の機能解析

    上原 康昭, 長谷川 喜弘, 高橋 素子, McCormack Francis X.

    日本呼吸器学会誌   11 ( 増刊 )   44 - 44   2022.4

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  • METの糖鎖による機能制御メカニズムの解析

    齋藤 淳, 長谷川 喜弘, 藤谷 直樹, 有木 茂, 上原 康昭, 松本 邦夫, 高橋 素子

    日本生化学会大会プログラム・講演要旨集   94回   [1T13m - 014)]   2021.11

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  • METの糖鎖による機能制御メカニズムの解析

    齋藤 淳, 長谷川 喜弘, 藤谷 直樹, 有木 茂, 上原 康昭, 松本 邦夫, 高橋 素子

    日本生化学会大会プログラム・講演要旨集   94回   [P - 04)]   2021.11

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  • METの糖鎖による機能制御メカニズムの解析

    齋藤 淳, 長谷川 喜弘, 藤谷 直樹, 有木 茂, 上原 康昭, 松本 邦夫, 高橋 素子

    日本生化学会大会プログラム・講演要旨集   94回   [1T13m - 014)]   2021.11

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  • Treatment of air leakage using the VIO soft coagulation system: a mouse pulmonary air leak model.

    Yuki Takahashi, Atsushi Saito, Yuji Sakuma, Makoto Tada, Ryunosuke Maki, Motoko Takahashi, Atsushi Watanabe

    Surgery today   51 ( 9 )   1521 - 1529   2021.9

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    PURPOSE: We aimed to compare the efficacy of the VIO soft coagulation system (VSCS) for the treatment of air leaks by sealing with fibrin glue, and also assess the histological alterations that occur after soft coagulation. METHODS: A mouse pulmonary air leak model was designed. The pulmonary fistula was subsequently coagulated with the VSCS or sealed with fibrin glue with polyglycolic acid (PGA) sheets. The burst pressure at air leak recurrence was measured in each group, and the results were compared. We also evaluated the histological alterations in the mouse pulmonary air leak model after soft coagulation with the VSCS. RESULTS: The burst pressure in the soft coagulation group (80 W/Effect 5) (median 42.8; range 35.4-53.8 cmH2O) was similar to that in the fibrin glue group (median 41.5; range 34.6-43.9 cmH2O) (p = 0.21). Histological examinations revealed that the visceral pleura remained torn, the structure of the pulmonary alveolus was maintained, and the coagulated fistula was covered with a fibrin membrane in the soft coagulation group. CONCLUSIONS: The pressure resistance following soft coagulation was equivalent to that after sealing using fibrin glue with PGA sheets. The air leaks were likely controlled by covering the fistula with a fibrin membrane after soft coagulation with the VSCS.

    DOI： 10.1007/s00595-021-02251-3

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  • Glycation in Disease

    Motoko Takahashi, Keiichiro Suzuki, Yoshitaka Ikeda, Naoyuki Taniguchi

    Comprehensive Glycoscience: Second Edition   119 - 132   2021.6

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    Language：English   Publishing type：Part of collection (book)   Publisher：Elsevier  

    DOI： 10.1016/B978-0-12-819475-1.00057-2

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  • Integrated Structural Analysis of N-Glycans and Free Oligosaccharides Allows for a Quantitative Evaluation of ER Stress. International journal

    Naoki Fujitani, Shigeru Ariki, Yoshihiro Hasegawa, Yasuaki Uehara, Atsushi Saito, Motoko Takahashi

    Biochemistry   60 ( 21 )   1708 - 1721   2021.6

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    Endoplasmic reticulum (ER) stress has been reported in a variety of diseases. Although ER stress can be detected using specific markers, it is still difficult to quantitatively evaluate the degree of stress and to identify the cause of the stress. The ER is the primary site for folding of secretory or transmembrane proteins as well as the site where glycosylation is initiated. This study therefore postulates that tracing the biosynthetic pathway of asparagine-linked glycans (N-glycans) would be a reporter for reflecting the state of the ER and serve as a quantitative descriptor of ER stress. Glycoblotting-assisted mass spectrometric analysis of the HeLa cell line enabled quantitative determination of the changes in the structures of N-glycans and degraded free oligosaccharides (fOSs) in response to tunicamycin- or thapsigargin-induced ER stress. The integrated analysis of neutral and sialylated N-glycans and fOSs showed the potential to elucidate the cause of ER stress, which cannot be readily done by protein markers alone. Changes in the total amount of glycans, increase in the ratio of high-mannose type N-glycans, increase in fOSs, and changes in the ratio of sialylated N-glycans in response to ER stress were shown to be potential descriptors of ER stress. Additionally, drastic clearance of accumulated N-glycans was observed in thapsigargin-treated cells, which may suggest the observation of ER stress-mediated autophagy or ER-phagy in terms of glycomics. Quantitative analysis of N-glycoforms composed of N-glycans and fOSs provides the dynamic indicators reflecting the ER status and the promising strategies for quantitative evaluation of ER stress.

    DOI： 10.1021/acs.biochem.0c00969

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  • Maillard reaction in vivo and its relevance to diseases: editorial and dedication. International journal

    Motoko Takahashi, Naoyuki Taniguchi

    Glycoconjugate journal   38 ( 3 )   277 - 281   2021.6

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  • Pleiotropic Actions of Aldehyde Reductase (AKR1A). International journal

    Junichi Fujii, Takujiro Homma, Satoshi Miyata, Motoko Takahashi

    Metabolites   11 ( 6 )   2021.5

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    We provide an overview of the physiological roles of aldehyde reductase (AKR1A) and also discuss the functions of aldose reductase (AKR1B) and other family members when necessary. Many types of aldehyde compounds are cytotoxic and some are even carcinogenic. Such toxic aldehydes are detoxified via the action of AKR in an NADPH-dependent manner and the resulting products may exert anti-diabetic and anti-tumorigenic activity. AKR1A is capable of reducing 3-deoxyglucosone and methylglyoxal, which are reactive intermediates that are involved in glycation, a non-enzymatic glycosylation reaction. Accordingly, AKR1A is thought to suppress the formation of advanced glycation end products (AGEs) and prevent diabetic complications. AKR1A and, in part, AKR1B are responsible for the conversion of d-glucuronate to l-gulonate which constitutes a process for ascorbate (vitamin C) synthesis in competent animals. AKR1A is also involved in the reduction of S-nitrosylated glutathione and coenzyme A and thereby suppresses the protein S-nitrosylation that occurs under conditions in which the production of nitric oxide is stimulated. As the physiological functions of AKR1A are currently not completely understood, the genetic modification of Akr1a could reveal the latent functions of AKR1A and differentiate it from other family members.

    DOI： 10.3390/metabo11060343

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  • 臨床応用を目指した肺胞微石症の基礎および治療法の検討

    齋藤 充史, 高宮 里奈, 藤谷 直樹, 有木 茂, 黒沼 幸治, 千葉 弘文, 高橋 素子, 高橋 弘毅

    日本肺サーファクタント・界面医学会雑誌   51   32 - 33   2021.3

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  • 臨床応用を目指した肺胞微石症の基礎および治療法の検討

    齋藤 充史, 高宮 里奈, 藤谷 直樹, 有木 茂, 黒沼 幸治, 千葉 弘文, 高橋 素子, 高橋 弘毅

    日本肺サーファクタント・界面医学会雑誌   51   32 - 33   2021.3

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  • Acrolein in cigarette smoke attenuates the innate immune responses mediated by surfactant protein D. International journal

    Rina Takamiya, Motoko Takahashi, Toshitaka Maeno, Atsushi Saito, Masaki Kato, Takahiro Shibata, Koji Uchida, Shigeru Ariki, Miyako Nakano

    Biochimica et biophysica acta. General subjects   1864 ( 11 )   129699 - 129699   2020.11

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    BACKGROUND: Surfactant proteins (SP) A and D belong to collectin family proteins, which play important roles in innate immune response in the lung. We previously demonstrated that cigarette smoke (CS) increases the acrolein modification of SP-A, thereby impairing the innate immune abilities of this protein. In this study, we focused on the effects of CS and its component, acrolein, on the innate immunity role of another collectin, SP-D. METHODS: To determine whether aldehyde directly affects SP-D, we examined the lungs of mice exposed to CS for 1 week and detected aldehyde-modified SP-D using an aldehyde reactive probe. The structural changes in CS extract (CSE) or acrolein-exposed recombinant human (h)SP-D were determined by western blot, liquid chromatography-electrospray ionization tandem mass spectrometry, and blue native-polyacrylamide gel electrophoresis analyses. Innate immune functions of SP-D were determined by bacteria growth and macrophage phagocytosis. RESULTS: Aldehyde-modified SP-D as well as SP-A was detected in the lungs of mice exposed to CS for 1 week. Exposure of hSP-D to CSE or acrolein induced an increased higher-molecular -weight of hSP-D and acrolein induced modification of five lysine residues in hSP-D. These modifications led to disruption of the multimer structure of SP-D and attenuated its ability to inhibit bacterial growth and activate macrophage phagocytosis. CONCLUSION: CS induced acrolein modification in SP-D, which in turn induced structural and functional defects in SP-D. GENERAL SIGNIFICANCE: These results suggest that CS-induced structural and functional defects in SP-D contribute to the dysfunction of innate immune responses in the lung following CS exposure.

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  • 膜タンパク質の構造制御と機能制御 増殖因子受容体の糖鎖の構造と機能

    高橋 素子, 藤谷 直樹, 長谷川 喜弘, 上原 康昭, 姚 閔

    日本生化学会大会プログラム・講演要旨集   93回   [2S04a - 04]   2020.9

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  • METの部位特異的糖鎖構造の解析

    齋藤 淳, 横山 早織, 藤谷 直樹, 齋藤 充史, 有木 茂, 千葉 弘文, 高橋 弘毅, 高橋 素子

    日本呼吸器学会誌   9 ( 増刊 )   303 - 303   2020.8

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  • METの部位特異的糖鎖構造の解析

    齋藤 淳, 横山 早織, 藤谷 直樹, 齋藤 充史, 有木 茂, 千葉 弘文, 高橋 弘毅, 高橋 素子

    日本呼吸器学会誌   9 ( 増刊 )   303 - 303   2020.8

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  • 肺MAC症における血清L-Ficolinの意義

    黒沼 幸治, 小林 智史, 斎藤 充史, 池田 貴美之, 大塚 満雄, 千葉 弘文, 有木 茂, 高橋 素子, 高橋 弘毅

    分子呼吸器病   24 ( 1 )   84 - 87   2020.3

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  • Insufficient serum L-ficolin is associated with disease presence and extent of pulmonary Mycobacterium avium complex disease. Reviewed International journal

    Kobayashi T, Kuronuma K, Saito A, Ikeda K, Ariki S, Saitou A, Otsuka M, Chiba H, Takahashi S, Takahashi M, Takahashi H

    Respiratory research   20 ( 1 )   224 - 224   2019.10

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    BACKGROUND: The incidence of infectious disease caused by nontuberculous mycobacteria is increasing worldwide. Pulmonary Mycobacterium avium complex (MAC) disease is difficult to treat with chemotherapy, and its mechanism of infection, infection route, disease onset, and severity remain unknown. Ficolins are oligomeric defense lectins. L-ficolin plays an important role in innate immunity. This study's aim was to identify L-ficolin's role in patients with pulmonary MAC disease. METHODS: Between April 2011 and September 2017, 61 Japanese patients with pulmonary MAC disease were seen at our hospital. A control group, comprising 30 healthy individuals, without respiratory disease were enrolled in our study. The relationship between serum L-ficolin levels and disease severity was assessed, and L-ficolin's antibacterial role was examined. RESULTS: Serum L-ficolin levels were significantly lower in patients with pulmonary MAC disease than in healthy subjects (1.69 ± 1.27 μg/ml vs. 3.96 ± 1.42 μg/ml; p < 0.001). The cut-off value, based on receiver operating characteristic (ROC) analysis results, was 2.48 μg/ml (area under the curve (AUC) 0.90, sensitivity and specificity 83.6 and 86.7%, respectively). Serum L-ficolin levels were significantly lower in the patients with nodular bronchiectatic type disease compared with the patients with fibrocavitary type disease and were lower in the high-resolution computed tomography high-scoring group compared with low-scoring group. An in vitro analysis showed that purified recombinant L-ficolin bound to M. avium and its major cell wall component, lipoarabinomannan, in a concentration-dependent manner. In addition, recombinant L-ficolin suppressed M. avium growth in a concentration-dependent manner. CONCLUSIONS: Insufficient serum L-ficolin is associated with disease progression in pulmonary MAC disease, and the level of serum L-ficolin is a possible biomarker. TRIAL REGISTRATION: This study is registered with UMIN ( UMIN000022392 ).

    DOI： 10.1186/s12931-019-1185-9

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  • ErbB3の糖鎖による物性制御メカニズム

    高橋 素子, 加藤 公児, 藤谷 直樹, 斎藤 充史, 和田 芳直, 姚 閔

    日本生化学会大会プログラム・講演要旨集   92回   [1T10m - 01]   2019.9

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  • サーファクタントタンパク質Aによる尿路病原性大腸菌の排除機構

    有木 茂, 齋藤 充史, 高宮 里奈, 高橋 素子

    日本生化学会大会プログラム・講演要旨集   92回   [3P - 338]   2019.9

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  • タバコ煙中のacroleinによる肺サーファクタントタンパク質D(SP-D)の構造、機能への影響

    高宮 里奈, 有木 茂, 前野 敏孝, 齋藤 充史, 高橋 弘毅, 高橋 素子, 中の 三弥子

    日本生化学会大会プログラム・講演要旨集   92回   [1T10m - 05]   2019.9

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  • ErbB3の糖鎖による物性制御メカニズム

    高橋 素子, 加藤 公児, 藤谷 直樹, 斎藤 充史, 和田 芳直, 姚 閔

    日本生化学会大会プログラム・講演要旨集   92回   [1T10m - 01]   2019.9

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  • タバコ煙中のアクロレインが肺サーファクタントタンパク質A(SP-A)に及ぼす影響

    高宮 里奈, 前野 敏孝, 有木 茂, 齋藤 充史, 高橋 弘毅, 黒木 由夫, 高橋 素子

    分子呼吸器病   23 ( 1 )   68 - 72   2019.3

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  • びまん性肺疾患の基礎研究 臨床応用を目指した肺胞微石症の基礎および治療法の検討

    齋藤 充史, 齋藤 淳, 藤谷 直樹, 有木 茂, 高橋 素子, 高橋 弘毅

    日本呼吸器学会誌   8 ( 増刊 )   164 - 164   2019.3

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  • Life-style related disease and aging

    Kazuaki Ohtsubo, Yasuhiko Kizuka, Naoyuki Taniguchi, Motoko Takahashi, Katsuhiko Yanagisawa, Shinobu Kitazume, Koichi Furukawa, Yuhsuke Ohmi, Keiko Furukawa, Yoshihiro Akimoto

    Glycoscience: Basic Science to Applications: Insights from the Japan Consortium for Glycobiology and Glycotechnology (JCGG)   269 - 288   2019.1

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    DOI： 10.1007/978-981-13-5856-2_16

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  • Hydrogen atom attachment to histidine and tryptophan containing peptides in the gas phase Reviewed

    Physical Chemistry Chemical Physics   2019

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    &lt;p&gt;In this study, we focus on the gas-phase fragmentation induced by the attachment of hydrogen atoms to the histidine and tryptophan residue side-chains in the peptide that provides the fragment ions due to C&lt;sub&gt;α&lt;/sub&gt;–C&lt;sub&gt;β&lt;/sub&gt; bond cleavage.&lt;/p&gt;

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  • Comparison of immune response in mice sensitized to an animal allergen, Can f 1, and to a food allergen, ovalbumin.

    Noriko Tosa, Kumiko Yoshimatsu, Motoko Takahashi, Jiro Arikawa

    Biomedical research (Tokyo, Japan)   40 ( 1 )   9 - 15   2019

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    Can f 1 belongs to the lipocalin superfamily and is considered to be an animal allergen. The immune response induced by Can f 1 in mice was compared with that induced by ovalbumin (OVA), a typical food allergen. Female BALB/c and C57BL/6 mice (6 weeks of age) were subcutaneously injected with Can f 1 or OVA with or without aluminum hydroxide (Alum) three times with intervals of two weeks. Serum levels of total IgE or antigen-specific IgE and production of IL13 and IFNγ from splenocytes were analyzed. Immunization with Can f 1 or OVA increased serum levels of both total IgE and antigen-specific IgE significantly irrespective of Alum. These results indicate that Can f 1 and OVA were able to induce allergic sensitization in mice. Splenocyte production of IL13 in mice immunized with Can f 1 or OVA with and without Alum were significantly increased after stimulation with each antigen. However, IL13 levels in the mice immunized with Can f 1 with Alum were significantly lower than those immunized without Alum. Increases in IFNγ levels after stimulation with Can f 1 or OVA were not remarkable. No influence of genetic backgrounds of BALB/c and C57BL/6 mice was found. Although Can f 1 induced Th2 type immune responses as was also the case for immunization with OVA, an inhibitory effect of Alum on induction of IL13 was observed only in mice immunized with Can f 1. These results suggest that the immune mechanism for allergic sensitization with Can f 1 is different from that with OVA.

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  • Mice deficient in aldo-keto reductase 1a (Akr1a) are resistant to thioacetamide-induced liver injury. Reviewed International journal

    Takujiro Homma, Takaya Shirato, Ryusuke Akihara, Sho Kobayashi, Jaeyong Lee, Ken-Ichi Yamada, Satoshi Miyata, Motoko Takahashi, Junichi Fujii

    Toxicology letters   294   37 - 43   2018.9

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    Aldehyde reductase (Akr1a) has been reported to be involved in detoxification of reactive aldehydes as well as in the synthesis of bioactive compounds such as ascorbic acid (AsA). Because Akr1a is expressed at high levels in the liver and is involved in xenobiotic metabolism, our objective was to investigate the hepato-protective role of Akr1a in a thioacetamide (TAA)-induced hepatotoxicity model using Akr1a-deficient (Akr1a-/-) mice. Wild-type (WT) and Akr1a-/- mice were injected intraperitoneally with TAA and the extent of liver injury in the acute phase was assessed. Intriguingly, the extent of TAA-induced liver damage was less in the Akr1a-/- mice than in the WT mice. Biomarkers for the ER stress-induced apoptosis pathway were markedly decreased in the livers of Akr1a-/- mice, whereas AsA levels in plasma did not change significantly in any of the mice. In the liver, TAA is converted to reactive metabolites such as TAA S-oxide and then to TAA S, S-dioxide via the action of CYP2E1. In Akr1a-/- mice, CYP2E1 activity was relatively lower than WT mice at the basal level, leading to reactive TAA metabolites being produced at lower levels after the TAA treatment. The levels of liver proteins that were modified with these metabolites were also lower in the Akr1a-/- mice than the WT mice after the TAA treatment. Furthermore, after a lethal dose of a TAA challenge, the WT mice all died within 36 h, whereas almost all of the Akr1a-/- mice survived. These collective results suggest that Akr1a-/- mice are resistant to TAA-induced liver injury, and it follows that the absence of Akr1a might modulate TAA bioactivation.

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  • ErbB4の糖鎖による機能制御メカニズム

    高橋 素子, 和田 芳直, 浅川 大樹, 有木 茂, 高宮 里奈, 齋藤 充史

    日本生化学会大会プログラム・講演要旨集   91回   [1T11a - 037)]   2018.9

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  • EGFR遺伝子変異陽性肺腺癌患者における予後予測因子としてのSP-Dの有用性

    梅田 泰淳, 長谷川 喜弘, 大塚 満雄, 黒沼 幸治, 高橋 素子, 高橋 弘毅

    日本内科学会雑誌   107 ( Suppl. )   176 - 176   2018.2

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  • Impaired diversity of the lung microbiome predicts progression of idiopathic pulmonary fibrosis. Reviewed International journal

    Takahashi Y, Saito A, Chiba H, Kuronuma K, Ikeda K, Kobayashi T, Ariki S, Takahashi M, Sasaki Y, Takahashi H

    Respiratory research   19 ( 1 )   34 - 34   2018.2

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    BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is the most frequent and severe form of idiopathic interstitial pneumonias. Although IPF has not been thought to be associated with bacterial communities, recent papers reported the possible role of microbiome composition in IPF. The roles of microbiomes in respiratory functions and as clinical biomarkers for IPF remain unknown. In this study, we aim to identify the relationship between the microbial environment in the lung and clinical findings. METHODS: Thirty-four subjects diagnosed with IPF were included in this analysis. The 16S rDNA was purified from bronchoalveolar lavage fluid obtained at the time of diagnosis and analyzed using next-generation sequencing techniques to characterize the bacterial communities. Furthermore, microbiomes from mice with bleomycin-induced lung fibrosis were analyzed. RESULTS: The most prevalent lung phyla were Firmicutes, Proteobacteria and Bacteroidetes. Decreased microbial diversity was found in patients with low forced vital capacity (FVC) and early mortality. Additionally, the diversity and relative abundance of Firmicutes, Streptococcaceae, and Veillonellaceae were significantly associated with FVC, 6-min walk distance, and serum surfactant protein D. Bleomycin-induced lung fibrosis resulted in decrease of diversity and alteration of microbiota in PCoA analysis. These results support the observations in human specimens. CONCLUSIONS: This study identified relationships between specific taxa in BALF and clinical findings, which were also supported by experiments in a mouse model. Our data suggest the possibility that loss of microbial diversity is associated with disease activities of IPF.

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  • タバコ煙中のアクロレインが肺サーファクタントタンパク質A(SP-A)の機能や構造に及ぼす影響

    高宮 里奈, 内田 浩二, 柴田 貴広, 前野 敏孝, 有木 茂, 長谷川 喜弘, 齊藤 充史, 黒木 由夫, 高橋 素子

    生命科学系学会合同年次大会   2017年度   [3P - 1166]   2017.12

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  • 肺サーファクタントタンパク質Dは変異型EGFRの活性化を阻害し、肺腺がんの進展を抑制する

    長谷川 喜弘, 梅田 泰淳, 大塚 満雄, 有木 茂, 高宮 里奈, 齋藤 充史, 高橋 弘毅, 黒木 由夫, 高橋 素子

    生命科学系学会合同年次大会   2017年度   [1P - 0948]   2017.12

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  • Surfactant protein A down-regulates epidermal growth factor receptor by mechanisms different from those of surfactant protein D Reviewed

    Yoshihiro Hasegawa, Motoko Takahashi, Shigeru Ariki, Atsushi Saito, Yasuaki Uehara, Rina Takamiya, Koji Kuronuma, Hirofumi Chiba, Yuji Sakuma, Hiroki Takahashi, Yoshio Kuroki

    JOURNAL OF BIOLOGICAL CHEMISTRY   292 ( 45 )   18565 - 18576   2017.11

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    DOI： 10.1074/jbc.M117.800771

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  • Surfactant protein D inhibits activation of non-small cell lung cancer-associated mutant EGFR and affects clinical outcomes of patients Reviewed

    Y. Umeda, Y. Hasegawa, M. Otsuka, S. Ariki, R. Takamiya, A. Saito, Y. Uehara, H. Saijo, K. Kuronuma, H. Chiba, H. Ohnishi, Y. Sakuma, H. Takahashi, Y. Kuroki, M. Takahashi

    ONCOGENE   36 ( 46 )   6432 - 6445   2017.11

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    DOI： 10.1038/onc.2017.253

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  • ACSL3 promotes intratumoral steroidogenesis in prostate cancer cells. Reviewed International journal

    Migita T, Takayama KI, Urano T, Obinata D, Ikeda K, Soga T, Takahashi S, Inoue S

    Cancer Sci.   108 ( 10 )   2011 - 2021   2017.10

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    Long-chain acyl-coenzyme A (CoA) synthetase 3 (ACSL3) is an androgen-responsive gene involved in the generation of fatty acyl-CoA esters. ACSL3 is expressed in both androgen-sensitive and castration-resistant prostate cancer (CRPC). However, its role in prostate cancer remains elusive. We overexpressed ACSL3 in androgen-dependent LNCaP cells and examined the downstream effectors of ACSL3. Furthermore, we examined the role of ACSL3 in the androgen metabolism of prostate cancer. ACSL3 overexpression led to upregulation of several genes such as aldo-keto reductase 1C3 (AKR1C3) involved in steroidogenesis, which utilizes adrenal androgen dehydroepiandrosterone sulfate (DHEAS) as substrate, and downregulated androgen-inactivating enzyme UDP-glucuronosyltransferase 2 (UGT2B). Exposure to DHEAS significantly increased testosterone levels and cell proliferative response in ACSL3-overexpressing cells when compared to that in control cells. A public database showed that ACSL3 level was higher in CRPC than in hormone-sensitive prostate cancer. CRPC cells showed an increased expression of ACSL3 and an expression pattern of AKR1C3 and UGT2B similar to ACSL3-overexpressing cells. DHEAS stimulation significantly promoted the proliferation of CRPC cells when compared to that of LNCaP cells. These findings suggest that ACSL3 contributes to the growth of CRPC through intratumoral steroidogenesis (i.e. promoting androgen synthesis from DHEAS and preventing the catabolism of active androgens).

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  • Disruption of the structural and functional features of surfactant protein A by acrolein in cigarette smoke Reviewed

    Rina Takamiya, Koji Uchida, Takahiro Shibata, Toshitaka Maeno, Masaki Kato, Yoshiki Yamaguchi, Shigeru Ariki, Yoshihiro Hasegawa, Atsushi Saito, Soichi Miwa, Hiroki Takahashi, Takaaki Akaike, Yoshio Kuroki, Motoko Takahashi

    SCIENTIFIC REPORTS   7 ( 1 )   8304   2017.8

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    DOI： 10.1038/s41598-017-08588-5

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  • Surfactant Protein A Inhibits Growth and Adherence of Uropathogenic Escherichia coli To Protect the Bladder from Infection Reviewed

    Jiro Hashimoto, Motoko Takahashi, Atsushi Saito, Masaki Murata, Yuichiro Kurimura, Chiaki Nishitani, Rina Takamiya, Yasuaki Uehara, Yoshihiro Hasegawa, Yoshiki Hiyama, Norimasa Sawada, Satoshi Takahashi, Naoya Masumori, Yoshio Kuroki, Shigeru Ariki

    JOURNAL OF IMMUNOLOGY   198 ( 7 )   2898 - 2905   2017.4

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    DOI： 10.4049/jimmunol.1502626

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  • Surfactant protein A (SP-A) and SP-A-derived peptide attenuate chemotaxis of mast cells induced by human beta-defensin 3 Reviewed

    Yasuaki Uehara, Motoko Takahashi, Masaki Murata, Atsushi Saito, Rina Takamiya, Yoshihiro Hasegawa, Koji Kuronuma, Hirofumi Chiba, Jiro Hashimoto, Norimasa Sawada, Hiroki Takahashi, Yoshio Kuroki, Shigeru Ariki

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   485 ( 1 )   107 - 112   2017.3

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    DOI： 10.1016/j.bbrc.2017.02.028

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  • N-glycans of growth factor receptors: their role in receptor function and disease implications Reviewed

    Motoko Takahashi, Yoshihiro Hasegawa, Congxiao Gao, Yoshio Kuroki, Naoyuki Taniguchi

    CLINICAL SCIENCE   130 ( 20 )   1781 - 1792   2016.10

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  • 肺サーファクタント蛋白質Dによる変異型EGFRの制御機構

    長谷川 喜弘, 佐久間 裕司, 高橋 素子

    日本癌学会総会記事   75回   J - 3044   2016.10

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  • Disease-associated glycans on cell surface proteins Reviewed

    Motoko Takahashi, Yasuhiko Kizuka, Kazuaki Ohtsubo, Jianguo Gu, Naoyuki Taniguchi

    MOLECULAR ASPECTS OF MEDICINE   51   56 - 70   2016.10

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  • Glycation vs. glycosylation: a tale of two different chemistries and biology in Alzheimer's disease Reviewed

    Naoyuki Taniguchi, Motoko Takahashi, Yasuhiko Kizuka, Shinobu Kitazume, Vladimir V. Shuvaev, Tomomi Ookawara, Akiko Furuta

    GLYCOCONJUGATE JOURNAL   33 ( 4 )   487 - 497   2016.8

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  • SP-AおよびSP-A由来ペプチドはヒトβ-デフェンシン3による肥満細胞の遊走を抑制する

    有木 茂, 上原 康昭, 村田 雅樹, 高宮 里奈, 長谷川 喜弘, 斎藤 充史, 千葉 弘文, 黒沼 幸治, 高橋 素子, 高橋 弘毅, 黒木 由夫

    分子呼吸器病   20 ( 1 )   120 - 123   2016.3

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  • Proteomic and glycomic analyses of a lung-specific protein surfactant protein-D Reviewed

    Emi Ito, Ritsuko Oka, Takeo Ishii, Hiroaki Korekane, Ayako Kurimoto, Yasuhiko Kizuka, Shinobu Kitazume, Shigeru Ariki, Motoko Takahashi, Yoshio Kuroki, Kozui Kida, Naoyuki Taniguchi

    Data in Brief   5   707 - 711   2015.12

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    DOI： 10.1016/j.dib.2015.09.017

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  • 肺コレクチンSP-Aによる肺胞マクロファージの分化調節機構の解明

    高宮 里奈, 有木 茂, 村田 雅樹, 長谷川 喜弘, 高橋 素子, 澤田 典均, 黒木 由夫

    日本生化学会大会・日本分子生物学会年会合同大会講演要旨集   88回・38回   [2T特 - 10(2P0275)]   2015.12

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  • 肺サーファクタント蛋白質AおよびDによるEGFRの機能制御メカニズム

    長谷川 喜弘, 高橋 素子

    日本癌学会総会記事   74回   J - 1206   2015.10

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  • Fucosylated surfactant protein-D is a biomarker candidate for the development of chronic obstructive pulmonary disease Reviewed

    Emi Ito, Ritsuko Oka, Takeo Ishii, Hiroaki Korekane, Ayako Kurimoto, Yasuhiko Kizuka, Shinobu Kitazume, Shigeru Ariki, Motoko Takahashi, Yoshio Kuroki, Kozui Kida, Naoyuki Taniguchi

    Journal of Proteomics   127 ( Pt B )   386 - 394   2015.9

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    DOI： 10.1016/j.jprot.2015.07.011

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  • Surfactant protein D suppresses lung cancer progression by downregulation of epidermal growth factor signalling (vol 34, pg 838, 2014) Reviewed

    Y. Hasegawa, M. Takahashi, S. Ariki, D. Asakawa, M. Tajiri, Y. Wada, Y. Yamaguchi, C. Nishitani, R. Takamiya, A. Saito, Y. Uehara, J. Hashimoto, Y. Kurimura, H. Takahashi, Y. Kuroki

    ONCOGENE   34 ( 32 )   4285 - 4286   2015.8

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  • Surfactant protein D suppresses lung cancer progression by downregulation of epidermal growth factor signaling Reviewed

    Y. Hasegawa, M. Takahashi, S. Ariki, D. Asakawa, M. Tajiri, Y. Wada, Y. Yamaguchi, C. Nishitani, R. Takamiya, A. Saito, Y. Uehara, J. Hashimoto, Y. Kurimura, H. Takahashi, Y. Kuroki

    ONCOGENE   34 ( 7 )   838 - 845   2015.2

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    DOI： 10.1038/onc.2014.20

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  • Functional Regulation of ErbB Receptors by N-Glycans Reviewed

    Motoko Takahashi

    Glycoscience: Biology and Medicine   983 - 990   2015.1

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    DOI： 10.1007/978-4-431-54841-6_55

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  • Glycation of Proteins Reviewed

    Motoko Takahashi

    Glycoscience: Biology and Medicine   1339 - 1345   2015.1

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    DOI： 10.1007/978-4-431-54841-6_182

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  • The single N-glycan deletion mutant of soluble ErbB3 protein attenuates heregulin beta 1-induced tumor progression by blocking of the HIF-1 and Nrf2 pathway Reviewed

    Rina Takamiya, Motoko Takahashi, Yasuaki Uehara, Shigeru Ariki, Jiro Hashimoto, Yoshihiro Hasegawa, Yoshio Kuroki

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   454 ( 3 )   364 - 368   2014.11

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    DOI： 10.1016/j.bbrc.2014.10.086

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  • 肺コレクチンの単球機能への影響

    高宮 里奈, 村田 雅樹, 上原 康昭, 有木 茂, 長谷川 喜弘, 橋本 次朗, 高橋 素子, 澤田 典均, 黒木 由夫

    日本生化学会大会プログラム・講演要旨集   87回   [2T16a - 01]   2014.10

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  • 肺サーファクタント蛋白質AとDによるEGFシグナルの抑制作用

    長谷川 喜弘, 高橋 素子, 有木 茂, 高宮 里奈, 上原 康昭, 橋本 次朗, 浅川 大樹, 田尻 道子, 和田 芳直, 高橋 弘毅, 黒木 由夫

    日本生化学会大会プログラム・講演要旨集   87回   [2T15a - 14]   2014.10

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  • Reductive detoxification of acrolein as a potential role for aldehyde reductase (AKR1A) in mammals. Reviewed International journal

    Toshihiro Kurahashi, Myoungsu Kwon, Takujiro Homma, Yuka Saito, Jaeyong Lee, Motoko Takahashi, Ken-Ichi Yamada, Satoshi Miyata, Junichi Fujii

    Biochemical and biophysical research communications   452 ( 1 )   136 - 41   2014.9

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    Aldehyde reductase (AKR1A), a member of the aldo-keto reductase superfamily, suppresses diabetic complications via a reduction in metabolic intermediates; it also plays a role in ascorbic acid biosynthesis in mice. Because primates cannot synthesize ascorbic acid, a principle role of AKR1A appears to be the reductive detoxification of aldehydes. In this study, we isolated and immortalized mouse embryonic fibroblasts (MEFs) from wild-type (WT) and human Akr1a-transgenic (Tg) mice and used them to investigate the potential roles of AKR1A under culture conditions. Tg MEFs showed higher methylglyoxal- and acrolein-reducing activities than WT MEFs and also were more resistant to cytotoxicity. Enzymatic analyses of purified rat AKR1A showed that the efficiency of the acrolein reduction was about 20% that of glyceraldehyde. Ascorbic acid levels were quite low in the MEFs, and while the administration of ascorbic acid to the cells increased the intracellular levels of ascorbic acid, it had no affect on the resistance to acrolein. Endoplasmic reticulum stress and protein carbonylation induced by acrolein treatment were less evident in Tg MEFs than in WT MEFs. These data collectively indicate that one of the principle roles of AKR1A in primates is the reductive detoxification of aldehydes, notably acrolein, and protection from its detrimental effects.

    DOI： 10.1016/j.bbrc.2014.08.072

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  • MicroRNA-31 expression in relation to BRAF mutation, CpG island methylation and colorectal continuum in serrated lesions. Reviewed International journal

    Ito M, Mitsuhashi K, Igarashi H, Nosho K, Naito T, Yoshii S, Takahashi H, Fujita M, Sukawa Y, Yamamoto E, Takahashi T, Adachi Y, Nojima M, Sasaki Y, Shinomura Y

    International journal of cancer   135 ( 11 )   2507 - 15   2014.4

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    The CpG island methylator phenotype (CIMP) is a distinct form of epigenomic instability. Many CIMP-high colorectal cancers (CRCs) with BRAF mutation are considered to arise from serrated pathway. We recently reported that microRNA-31 (miR-31) is associated with BRAF mutation in colorectal tumors. Emerging new approaches have revealed gradual changes in BRAF mutation and CIMP-high throughout the colorectum in CRCs. Here, we attempted to identify a possible association between miR-31 and epigenetic features in serrated pathway, and hypothesized that miR-31 supports the "colorectal continuum" concept. We evaluated miR-31 expression, BRAF mutation and epigenetic features including CIMP status in 381 serrated lesions and 222 non-serrated adenomas and examined associations between them and tumor location (rectum; sigmoid, descending, transverse and ascending colon and cecum). A significant association was observed between high miR-31 expression and CIMP-high status in serrated lesions with BRAF mutation (p = 0.0001). In contrast, miR-31 was slightly but insignificantly associated with CIMP status in the cases with wild-type BRAF. miR-31 expression in sessile serrated adenomas (SSAs) with cytological dysplasia was higher than that in SSAs, whereas, no significant difference was observed between traditional serrated adenomas (TSAs) and TSAs with high-grade dysplasia. The frequency of miR-31, BRAF mutation CIMP-high and MLH1 methylation increased gradually from the rectum to cecum in serrated lesions. In conclusion, miR-31 expression was associated with CIMP-high status in serrated lesions with BRAF mutation. Our data also suggested that miR-31 plays an important role in SSA evolution and may be a molecule supporting the colorectal continuum.

    DOI： 10.1002/ijc.28920

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  • A Circadian Clock Gene, Rev-erb alpha, Modulates the Inflammatory Function of Macrophages through the Negative Regulation of Ccl2 Expression Reviewed

    Shogo Sato, Takuya Sakurai, Junetsu Ogasawara, Motoko Takahashi, Tetsuya Izawa, Kazuhiko Imaizumi, Naoyuki Taniguchi, Hideki Ohno, Takako Kizaki

    JOURNAL OF IMMUNOLOGY   192 ( 1 )   407 - 417   2014.1

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    DOI： 10.4049/jimmunol.1301982

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  • Ascorbic acid reverses the prolonged anesthetic action of pentobarbital in Akr1a-knockout mice Reviewed

    Junitsu Ito, Noriyuki Otsuki, Xuhong Zhang, Tasuku Konno, Toshihiro Kurahashi, Motoko Takahashi, Mayumi Yamato, Yuta Matsuoka, Ken-ichi Yamada, Satoshi Miyata, Junichi Fujii

    LIFE SCIENCES   95 ( 1 )   1 - 8   2014.1

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    DOI： 10.1016/j.lfs.2013.12.004

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  • Suppression of heregulin β signaling by the single N-glycan deletion mutant of soluble ErbB3 protein Reviewed

    Motoko Takahashi, Yoshihiro Hasegawa, Yoshitaka Ikeda, Yoshinao Wada, Michiko Tajiri, Shigeru Ariki, Rina Takamiya, Chiaki Nishitani, Motoko Araki, Yoshiki Yamaguchi, Naoyuki Taniguchi, Yoshio Kuroki

    Journal of Biological Chemistry   288 ( 46 )   32910 - 32921   2013.11

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    DOI： 10.1074/jbc.M113.491902

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  • Detection of N-glycolyated gangliosides in non-small-cell lung cancer using GMR8 monoclonal antibody Reviewed

    Nobuyoshi Hayashi, Hirofumi Chiba, Koji Kuronuma, Shinji Go, Yoshihiro Hasegawa, Motoko Takahashi, Shinsei Gasa, Atsushi Watanabe, Tadashi Hasegawa, Yoshio Kuroki, Jinichi Inokuchi, Hiroki Takahashi

    CANCER SCIENCE   104 ( 1 )   43 - 47   2013.1

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    DOI： 10.1111/cas.12027

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  • SURFACTANT PROTEINS A AND D SUPPRESS EPIDERMAL GROWTH FACTOR SIGNALING THROUGH INTERACTIONS WITH N-GLYCANS OF RECEPTOR Reviewed

    Hasegawa Yoshihiro, Takahashi Motoko, Ariki Shigeru, Asakawa Daiki, Tajiri Michiko, Wada Yoshinao, Takamiya Rina, Uehara Yasuaki, Hashimoto Jiro, Takahashi Hiroki, Kuroki Yoshio

    Respirology   18   55   2013

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  • The Effects of Exercise Training on Obesity-Induced Dysregulated Expression of Adipokines in White Adipose Tissue Reviewed

    Takuya Sakurai, Junetsu Ogasawara, Takako Kizaki, Shogo Sato, Yoshinaga Ishibashi, Motoko Takahashi, Osamu Kobayashi, Shuji Oh-ishi, Junichi Nagasawa, Kazuto Takahashi, Hitoshi Ishida, Tetsuya Izawa, Hideki Ohno

    INTERNATIONAL JOURNAL OF ENDOCRINOLOGY   2013   801743   2013

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  • Surfactant Protein D Inhibits Adherence of Uropathogenic Escherichia coli to the Bladder Epithelial Cells and the Bacterium-induced Cytotoxicity A POSSIBLE FUNCTION IN URINARY TRACT Reviewed

    Yuichiro Kurimura, Chiaki Nishitani, Shigeru Ariki, Atsushi Saito, Yoshihiro Hasegawa, Motoko Takahashi, Jiro Hashimoto, Satoshi Takahashi, Taiji Tsukamoto, Yoshio Kuroki

    JOURNAL OF BIOLOGICAL CHEMISTRY   287 ( 47 )   39578 - 39588   2012.11

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    DOI： 10.1074/jbc.M112.380287

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  • In vivo role of aldehyde reductase

    Motoko Takahashi, Satoshi Miyata, Junichi Fujii, Yoko Inai, Shigemitsu Ueyama, Motoko Araki, Tomoyoshi Soga, Reiko Fujinawa, Chiaki Nishitani, Shigeru Ariki, Takeyuki Shimizu, Tomomi Abe, Yoshito Ihara, Morimitsu Nishikimi, Yasunori Kozutsumi, Naoyuki Taniguchi, Yoshio Kuroki

    BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS   1820 ( 11 )   1787 - 1796   2012.11

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    DOI： 10.1016/j.bbagen.2012.07.003

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  • In vivo role of aldehyde reductase. Reviewed

    Takahashi M, Miyata S, Fujii J, Inai Y, Ueyama S, Araki M, Soga T, Fujinawa R, Nishitani C, Ariki S, Shimizu T, Abe T, Ihara Y, Nishikimi M, Kozutsumi Y, Taniguchi N, Kuroki Y

    Biochimica et biophysica acta   1820 ( 11 )   1787 - 1796   2012.11

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  • Measurement of peroxiredoxin-4 serum levels in rat tissue and its use as a potential marker for hepatic disease Reviewed

    Ritsu Ito, Motoko Takahashi, Hideyuki Ihara, Hiroki Tsukamoto, Junichi Fujii, Yoshitaka Ikeda

    MOLECULAR MEDICINE REPORTS   6 ( 2 )   379 - 384   2012.8

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    DOI： 10.3892/mmr.2012.935

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  • Pulmonary Surfactant Protein A Protects Lung Epithelium from Cytotoxicity of Human beta-Defensin 3 Reviewed

    Atsushi Saito, Shigeru Ariki, Hitoshi Sohma, Chiaki Nishitani, Kanako Inoue, Nobutaka Ebata, Motoko Takahashi, Yoshihiro Hasegawa, Koji Kuronuma, Hiroki Takahashi, Yoshio Kuroki

    JOURNAL OF BIOLOGICAL CHEMISTRY   287 ( 18 )   15034 - 15043   2012.4

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    DOI： 10.1074/jbc.M111.308056

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  • Pulmonary Collectins Play Distinct Roles in Host Defense against Mycobacterium avium Reviewed

    Shigeru Ariki, Takashi Kojima, Shinsei Gasa, Atsushi Saito, Chiaki Nishitani, Motoko Takahashi, Takeyuki Shimizu, Yuichiro Kurimura, Norimasa Sawada, Nobuhiro Fujii, Yoshio Kuroki

    JOURNAL OF IMMUNOLOGY   187 ( 5 )   2586 - 2594   2011.9

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    DOI： 10.4049/jimmunol.1100024

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  • Spontaneous skin damage and delayed wound healing in SOD1-deficient mice Reviewed

    Yoshihito Iuchi, Dipa Roy, Futoshi Okada, Noriko Kibe, Satoshi Tsunoda, Saori Suzuki, Motoko Takahashi, Hidekatsu Yokoyama, Jun Yoshitake, Seiji Kondo, Junichi Fujii

    MOLECULAR AND CELLULAR BIOCHEMISTRY   341 ( 1-2 )   181 - 194   2010.8

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    DOI： 10.1007/s11010-010-0449-y

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  • Pulmonary Collectins Protect Macrophages against Pore-forming Activity of Legionella pneumophila and Suppress Its Intracellular Growth Reviewed

    Kaku Sawada, Shigeru Ariki, Takashi Kojima, Atsushi Saito, Masami Yamazoe, Chiaki Nishitani, Takeyuki Shimizu, Motoko Takahashi, Hiroaki Mitsuzawa, Shin-ichi Yokota, Norimasa Sawada, Nobuhiro Fujii, Hiroki Takahashi, Yoshio Kuroki

    JOURNAL OF BIOLOGICAL CHEMISTRY   285 ( 11 )   8434 - 8443   2010.3

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    DOI： 10.1074/jbc.M109.074765

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  • Mannose binding lectin and lung collectins interact with Toll-like receptor 4 and MD-2 by different mechanisms Reviewed

    Takeyuki Shimizu, Chiaki Nishitani, Hiroaki Mitsuzawa, Shigeru Ariki, Motoko Takahashi, Katsuki Ohtani, Nobutaka Wakamiya, Yoshio Kuroki

    BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS   1790 ( 12 )   1705 - 1710   2009.12

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  • Mannose binding lectin and lung collectins interact with Toll-like receptor 4 and MD-2 by different mechanisms. Reviewed International journal

    Takeyuki Shimizu, Chiaki Nishitani, Hiroaki Mitsuzawa, Shigeru Ariki, Motoko Takahashi, Katsuki Ohtani, Nobutaka Wakamiya, Yoshio Kuroki

    Biochimica et biophysica acta   1790 ( 12 )   1705 - 10   2009.12

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    BACKGROUND: We have previously shown that lung collectins, surfactant protein A (SP-A) and surfactant protein D, interact with Toll-like receptor (TLR) 2, TLR4, or MD-2. Bindings of lung collectins to TLR2 and TLR4/MD-2 result in the alterations of signaling through these receptors, suggesting the immunomodulatory functions of lung collectins. Mannose binding lectin (MBL) is another collectin molecule which has structural homology to SP-A. The interaction between MBL and TLRs has not yet been determined. METHODS: We prepared recombinant MBL, and analyzed its bindings to recombinant soluble forms of TLR4 (sTLR4) and MD-2. RESULTS: MBL bound to sTLR4 and MD-2. The interactions were Ca2+-dependent and inhibited by mannose or monoclonal antibody against the carbohydrate-recognition domain of MBL. Treatment of sTLR4 or MD-2 by peptide N-glycosidase F significantly decreased the binding of MBL. SP-A bound to deglycosylated sTLR4, and this property did not change in chimeric molecules of SP-A/MBL in which Glu195-Phe228 or Thr174-Gly194 of SP-A were replaced with the corresponding MBL sequences. GENERAL SIGNIFICANCE: These results suggested that MBL binds to TLR4 and MD-2 through the carbohydrate-recognition domain, and that oligosaccharide moieties of TLR4 and MD-2 are important for recognition by MBL. Since our previous studies indicated that lung collectins bind to the peptide portions of TLRs, MBL and lung collectins interact with TLRs by different mechanisms. These direct interactions between MBL and TLR4 or MD-2 suggest that MBL may modulate cellular responses by altering signals through TLRs.

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  • Mutational analysis of Cys(88) of Toll-like receptor 4 highlights the critical role of MD-2 in cell surface receptor expression Reviewed

    Chiaki Nishitani, Motoko Takahashi, Hiroaki Mitsuzawa, Takeyuki Shimizu, Shigeru Ariki, Norio Matsushima, Yoshio Kuroki

    INTERNATIONAL IMMUNOLOGY   21 ( 8 )   925 - 934   2009.8

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  • Core fucose and bisecting GlcNAc, the direct modifiers of the N-glycan core: their functions and target proteins Reviewed

    Motoko Takahashi, Yoshio Kuroki, Kazuaki Ohtsubo, Naoyuki Taniguchi

    CARBOHYDRATE RESEARCH   344 ( 12 )   1387 - 1390   2009.8

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  • Core fucosylation of E-cadherin enhances cell-cell adhesion in human colon carcinoma WiDr cells Reviewed

    Daisuke Osumi, Motoko Takahashi, Eiji Miyoshi, Shunichi Yokoe, Seung Ho Lee, Katsuhisa Noda, Shoji Nakamori, Jianguo Gu, Yoshitaka Ikeda, Yoshio Kuroki, Kazuo Sengoku, Mutsuo Ishikawa, Naoyuki Taniguchi

    CANCER SCIENCE   100 ( 5 )   888 - 895   2009.5

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    DOI： 10.1111/j.1349-7006.2009.01125.x

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  • Pulmonary Surfactant Protein D Inhibits Lipopolysaccharide (LPS)-induced Inflammatory Cell Responses by Altering LPS Binding to Its Receptors Reviewed

    Masami Yamazoe, Chiaki Nishitani, Motoko Takahashi, Tsuyoshi Katoh, Shigeru Ariki, Takeyuki Shimizu, Hiroaki Mitsuzawa, Kaku Sawada, Dennis R. Voelker, Hiroki Takahashi, Yoshio Kuroki

    JOURNAL OF BIOLOGICAL CHEMISTRY   283 ( 51 )   35878 - 35888   2008.12

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  • Pulmonary Surfactant Protein D Binds MD-2 through the Carbohydrate Recognition Domain Reviewed

    Xiaomeng Nie, Chiaki Nishitani, Masami Yamazoe, Shigeru Ariki, Motoko Takahashi, Takeyuki Shimizu, Hiroaki Mitsuzawa, Kaku Sawada, Kelly Smith, Erika Crouch, Hisato Nagae, Hiroki Takahashi, Yoshio Kuroki

    BIOCHEMISTRY   47 ( 48 )   12878 - 12885   2008.12

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  • [Importance of core fucose in receptor function]. Reviewed

    Takahashi M, Miyoshi E, Gu J, Taniguchi N

    Tanpakushitsu kakusan koso. Protein, nucleic acid, enzyme   53 ( 12 Suppl )   1502 - 1507   2008.9

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  • Functional roles of N-glycans in cell signaling and cell adhesion in cancer Reviewed

    Yan-Yang Zhao, Motoko Takahashi, Jian-Guo Gu, Eiji Miyoshi, Akio Matsumoto, Shinobu Kitazume, Naoyuki Taniguchi

    CANCER SCIENCE   99 ( 7 )   1304 - 1310   2008.7

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  • N-glycan of ErbB family plays a crucial role in dimer formation and tumor promotion Reviewed

    Motoko Takahashi, Shunichi Yokoe, Michio Asahi, Seung Ho Lee, Wei Li, Daisuke Osumi, Eiji Miyoshi, Naoyuki Taniguchi

    BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS   1780 ( 3 )   520 - 524   2008.3

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  • N-glycan of ErbB family plays a crucial role in dimer formation and tumor promotion. Reviewed

    Takahashi M, Yokoe S, Asahi M, Lee SH, Li W, Osumi D, Miyoshi E, Taniguchi N

    Biochimica et biophysica acta   1780 ( 3 )   520 - 524   2008.3

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  • Gliclazide inhibits proliferation but stimulates differentiation of white and brown adipocytes Reviewed

    Norihiko Nakano, Nobuko Miyazawa, Takuya Sakurai, Takako Kizaki, Kiyoko Kimoto, Kazuto Takahashi, Hitoshi Ishida, Motoko Takahashi, Kenji Suzuki, Hideki Ohno

    JOURNAL OF BIOCHEMISTRY   142 ( 5 )   639 - 645   2007.11

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  • Pulmonary collectins in innate immunity of the lung Reviewed

    Yoshio Kuroki, Motoko Takahashi, Chiaki Nishitani

    CELLULAR MICROBIOLOGY   9 ( 8 )   1871 - 1879   2007.8

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  • Introduction of bisecting GlcNAc in N-glycans of adenylyl cyclase III enhances its activity Reviewed

    Wei Li, Motoko Takahashi, Yukinao Shibukawa, Shunichi Yokoe, Jianguo Gu, Eiji Miyoshi, Koichi Honke, Yoshitaka Ikeda, Naoyuki Taniguchi

    GLYCOBIOLOGY   17 ( 6 )   655 - 662   2007.6

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  • Acrolein induces cyclooxygenase-2 and prostaglandin production in human umbilical vein endothelial cells - Roles of p38 MAP kinase Reviewed

    Yong Seek Park, Jayoung Kim, Yoshiko Misonou, Rina Takamiya, Motoko Takahashi, Michael R. Freeman, Naoyuki Taniguchi

    ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY   27 ( 6 )   1319 - 1325   2007.6

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  • The Asn(418)-linked N-glycan of ErbB3 plays a crucial role in preventing spontaneous heterodimerization and tumor promotion Reviewed

    Shunichi Yokoe, Motoko Takahashi, Michio Asahi, Seung Ho Lee, Wei Li, Daisuke Osumi, Eiji Miyoshi, Naoyuki Taniguchi

    CANCER RESEARCH   67 ( 5 )   1935 - 1942   2007.3

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    DOI： 10.1158/0008-5472.CAN-06-3023

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  • Glycation and Disease Reviewed

    M. Takahashi, K. Suzuki, Y. Ikeda, N. Taniguchi

    Comprehensive Glycoscience: From Chemistry to Systems Biology   4-4   515 - 532   2007.1

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  • Glycosyltransferases and Glycosidases: Enzyme Mechanisms Reviewed

    Y. Ikeda, M. Takahashi

    Comprehensive Glycoscience: From Chemistry to Systems Biology   3-4   115 - 128   2007.1

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  • A secreted type of beta 1,6 N-acetylglucosaminyltransferase V (GnT-V), a novel angiogenesis inducer, is regulated by gamma-secretase Reviewed

    Susumu Nakahara, Takashi Saito, Nami Kondo, Kenta Moriwaki, Katsuhisa Noda, Shinji Ihara, Motoko Takahashi, Yoshihito Ide, Jianguo Gu, Hidenori Inohara, Taiichi Katayama, Masaya Tohyama, Takeshi Kubo, Naoyuki Taniguchi, Eiji Miyoshi

    FASEB JOURNAL   20 ( 14 )   2451 - 2459   2006.12

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  • A novel angiogenesis inducer, b1, 6-N-Acetylglucosaminyltransferase V (GnT-V), is processed as a secreted enzyme by g-secretase.

    Nakahara S, Saito T, Kondo N, Moriwaki K, Noda K, Ihara S, Takahashi M, Ide Y, Gu J, Inohara H, Katayama T, Tohyama M, Kubo T, Taniguchi N, Miyoshi E

    FASEB J   2006.6

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  • The Asn418-linked N-glycan of ErbB3 inhibits spontaneous heterodimerization with ErbB2, and suppresses anchorage dependent and independent cell growth through MAPK and PI3K/Akt pathways

    Yokoe S, Takahashi M, Asahi M, Osumi D, Gu J, Miyoshi E, Taniguchi N

    2006.6

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  • Loss of core fucosylation of low-density lipoprotein receptor-related protein-1 impairs its function, leading to the upregulation of serum levels of insulin-like growth factor-binding protein 3 in Fut8(-/-) mice Reviewed

    SH Lee, M Takahashi, K Honke, E Miyoshi, D Osumi, H Sakiyama, A Ekuni, XC Wang, S Inoue, JG Gu, K Kadomatsu, N Taniguchi

    JOURNAL OF BIOCHEMISTRY   139 ( 3 )   391 - 398   2006.3

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  • The internalization and metabolism of 3-deoxyglucosone in human umbilical vein endothelial cells Reviewed

    H Sakiyama, M Takahashi, T Yamamoto, T Teshima, SH Lee, Y Miyamoto, Y Misonou, N Taniguchi

    JOURNAL OF BIOCHEMISTRY   139 ( 2 )   245 - 253   2006.2

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  • Dysregulation of TGF-beta 1 receptor activation leads to abnormal lung development and emphysema-like phenotype in core fucose-deficient mice Reviewed

    XC Wang, S Inoue, JG Gu, E Miyoshi, K Noda, WZ Li, Y Mizuno-Horikawa, M Nakano, M Asahi, M Takahashi, N Uozumi, S Ihara, SH Lee, Y Ikeda, Y Yamaguchi, Y Aze, Y Tomiyama, J Fujii, K Suzuki, A Kondo, SD Shapiro, C Lopez-Otin, T Kuwaki, M Okabe, K Honke, N Taniguchi

    PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA   102 ( 44 )   15791 - 15796   2005.11

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    DOI： 10.1073/pnas.0507375102

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  • Assigned role of N-glycan of ErbB3

    Shunichi Yokoe, Motoko Takahashi, Michio Asahi, Jianguo Gu, Eiji Miyoshi, Naoyuki Taniguchi

    2005.10

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  • Acrolein induces Hsp72 via both PKC delta/JNK and calcium signaling pathways in human umbilical vein endothelial cells Reviewed

    Y Misonou, M Takahashi, YS Park, M Asahi, Y Miyamoto, H Sakiyama, XY Cheng, N Taniguchi

    FREE RADICAL RESEARCH   39 ( 5 )   507 - 512   2005.5

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  • Different immunoreactivity against monoclonal antibodies between wild-type and mutant copper/zinc superoxide dismutase linked to amyotrophic lateral sclerosis Reviewed

    N Fujiwara, Y Miyamoto, K Ogasahara, M Takahashi, T Ikegami, R Takamiya, K Suzuki, N Taniguchi

    JOURNAL OF BIOLOGICAL CHEMISTRY   280 ( 6 )   5061 - 5070   2005.2

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    DOI： 10.1074/jbc.M406106200

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  • Induction of thioredoxin reductase as an adaptive response to acrolein in human umbilical vein endothelial cells Reviewed

    YS Park, Y Misonou, N Fujiwara, M Takahashi, Y Miyamoto, YH Koh, K Suzuki, N Taniguchi

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   327 ( 4 )   1058 - 1065   2005.2

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    DOI： 10.1016/j.bbrc.2004.12.104

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  • Overexpression of mutated Cu,Zn-SOD in neuroblastoma cells results in cytoskeletal change Reviewed

    R Takamiya, M Takahashi, YS Park, Y Tawara, N Fujiwara, Y Miyamoto, JG Gu, K Suzuki, N Taniguchi

    AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY   288 ( 2 )   C253 - C259   2005.2

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    DOI： 10.1152/ajpcell.00014.2004

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  • The internalization of 3-deoxyglucosone in human umbilical vein endothelial cells Reviewed

    H. Sakiyama, M. Takahashi, T. Yamamoto, T. Teshima, N. Taniguchi

    Annals of the New York Academy of Sciences   1043 ( 1 )   933   2005

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    DOI： 10.1196/annals.1333.147

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  • A common pathway for intracellular reactive oxygen species production by glycoxidative and nitroxidative stress in vascular endothelial cells and smooth muscle cells Reviewed

    N Taniguchi, M Takahashi, H Sakiyama, YS Park, M Asahi, Y Misonou, Y Miyamoto

    MAILLARD REACTION: CHEMISTRY AT THE INTERFACE OF NUTRITION, AGING, AND DISEASE   1043   521 - 528   2005

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    DOI： 10.1196/annals.1333.059

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  • Pulmonary collectins enhance phagocytosis of mycobacterium avium through increased activity of mannose receptor Reviewed

    K Kudo, H Sano, H Takahashi, K Kuronuma, SI Yokota, N Fujii, KI Shimada, Yano, I, Y Kumazawa, DR Voelker, S Abe, Y Kuroki

    JOURNAL OF IMMUNOLOGY   172 ( 12 )   7592 - 7602   2004.6

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  • Introduction of bisecting GlcNAc into integrin alpha(5)beta(1) reduces ligand binding and down-regulates cell adhesion and cell migration Reviewed

    T Isaji, JG Gu, R Nishiuchi, YY Zhao, M Takahashi, E Miyoshi, K Honke, K Sekiguchi, N Taniguchi

    JOURNAL OF BIOLOGICAL CHEMISTRY   279 ( 19 )   19747 - 19754   2004.5

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    DOI： 10.1074/jbc.M311627200

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  • beta 1,4-N-Acetylglucosaminyltransferase III down-regulates neurite outgrowth induced by costimulation of epidermal growth factor and integrins through the Ras/ERK signaling pathway in PC12 cells Reviewed

    JG Gu, YY Zhao, T Isaji, Y Shibukawa, H Ihara, M Takahashi, Y Ikeda, E Miyoshi, K Honke, N Taniguchi

    GLYCOBIOLOGY   14 ( 2 )   177 - 186   2004.2

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  • Functional glycomics and evidence for gain- and loss-of-functions of target proteins for glycosyltransferases involved in N-glycan biosynthesis: their pivotal roles in growth and development, cancer metastasis and antibody therapy against cancer Reviewed

    N Taniguchi, JG Gu, M Takahashi, E Miyoshi

    PROCEEDINGS OF THE JAPAN ACADEMY SERIES B-PHYSICAL AND BIOLOGICAL SCIENCES   80 ( 2 )   82 - 91   2004.2

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  • Structural analysis of human alpha 1,6-fucosyltransferase Reviewed

    Ihara H, Toma S, Ikeda Y, Gu JG, Takahashi M, Miyoshi E, Tsukihara T, Nakagawa A, Taniguchi N

    Glycobiology   14 ( 11 )   1112 - 1113   2004

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  • Colocalization of polyol-metabolizing enzymes and immunological detection of fructated proteins in the female reproductive system of the rat Reviewed

    T Kaneko, Y Iuchi, M Takahashi, J Fujii

    HISTOCHEMISTRY AND CELL BIOLOGY   119 ( 4 )   309 - 315   2003.4

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    DOI： 10.1007/s00418-003-0516-5

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  • Glycation proceeds faster in mutated Cu, Zn-superoxide dismutases related to familial amyotrophic lateral sclerosis Reviewed

    R Takamiya, M Takahashi, T Myint, YS Park, N Miyazawa, T Endo, N Fujiwara, H Sakiyama, Y Misonou, Y Miyamoto, J Fujii, N Taniguchi

    FASEB JOURNAL   17 ( 3 )   938 - +   2003.3

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    DOI： 10.1096/fj.02-0768fje

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  • Down-regulation of hydrogen peroxide-induced PKC delta activation in N-acetylglucosaminyltransferase III-transfected HeLaS3 cells Reviewed

    Y Shibukawa, M Takahashi, Laffont, I, K Honke, N Taniguchi

    JOURNAL OF BIOLOGICAL CHEMISTRY   278 ( 5 )   3197 - 3203   2003.1

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    DOI： 10.1074/jbc.M207870200

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  • Identification of the binding site of methylglyoxal on glutathione peroxidase: Methylglyoxal inhibits glutathione peroxidase activity via binding to glutathione binding sites Arg 184 and 185 Reviewed

    YS Park, YH Koh, M Takahashi, Y Miyamoto, K Suzuki, N Dohmae, K Takio, K Honke, N Taniguchi

    FREE RADICAL RESEARCH   37 ( 2 )   205 - 211   2003

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    DOI： 10.1080/1071576021000041005

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  • Role of N-glycans in growth factor signaling Reviewed

    M Takahashi, T Tsuda, Y Ikeda, K Honke, N Taniguchi

    GLYCOCONJUGATE JOURNAL   20 ( 3 )   207 - 212   2003

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  • Localization and physiological implication of aldose reductase and sorbitol dehydrogenase in reproductive tracts and spermatozoa of male rats Reviewed

    T Kobayashi, T Kaneko, Y Iuchi, S Matsuki, M Takahashi, Sasagawa, I, T Nakada, J Fujii

    JOURNAL OF ANDROLOGY   23 ( 5 )   674 - 683   2002.9

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  • Apolipoprotein E activates Akt pathway in Neuro-2a in an isoform-specific manner Reviewed

    Laffont, I, M Takahashi, Y Shibukawa, K Honke, VV Shuvaev, G Siest, S Visvikis, N Taniguchi

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   292 ( 1 )   83 - 87   2002.3

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    DOI： 10.1006/bbrc.2002.6586

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  • Localization and physiological implication of polyol-metabolyzing enzymes in male and female reproductive systems of rat Reviewed

    J Fujii, T Kaneko, T Kobayashi, Y Iuchi, M Takahashi

    MAILLARD REACTION IN FOOD CHEMISTRY AND MEDICAL SCIENCE: UPDATE FOR THE POSTGENOMIC ERA   1245   363 - 364   2002

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  • Inactivation of thioredoxin reductase by acrolein Reviewed

    YS Park, N Fujiwara, YH Koh, M Takahashi, Y Miyamoto, K Suzuki, N Taniguchi

    MAILLARD REACTION IN FOOD CHEMISTRY AND MEDICAL SCIENCE: UPDATE FOR THE POSTGENOMIC ERA   1245   433 - 434   2002

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  • Osmotic stress induces HB-EGF gene expression via Ca2+/Pyk2/JNK signal cascades in rat aortic smooth muscle cells Reviewed

    YH Koh, WY Che, S Higashiyama, M Takahashi, Y Miyamoto, K Suzuki, N Taniguchi

    JOURNAL OF BIOCHEMISTRY   130 ( 3 )   351 - 358   2001.9

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  • Overexpression of N-acetylglucosaminyltransferase III enhances the epidermal growth factor-induced phosphorylation of ERK in HeLaS3 cells by up-regulation of the internalization rate of the receptors Reviewed

    Y Sato, M Takahashi, Y Shibukawa, SK Jain, R Hamaoka, J Miyagawa, Y Yaginuma, K Honke, M Ishikawa, N Taniguchi

    JOURNAL OF BIOLOGICAL CHEMISTRY   276 ( 15 )   11956 - 11962   2001.4

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    DOI： 10.1074/jbc.M008551200

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  • A glycomic approach to the identification and characterization of glycoprotein function in cells transfected with glycosyltransferase genes Reviewed

    N Taniguchi, A Ekuni, JH Ko, E Miyoshi, Y Ikeda, Y Ihara, A Nishikawa, K Honke, M Takahashi

    PROTEOMICS   1 ( 2 )   239 - 247   2001.2

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  • Cloning of amadoriase I isoenzyme from Aspergillus sp.: Evidence of FAD covalently linked to Cys342 Reviewed

    XL Wu, M Takahashi, SG Chen, VM Monnier

    BIOCHEMISTRY   39 ( 6 )   1515 - 1521   2000.2

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    DOI： 10.1021/bi992031g

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  • Glycosyltransferase genes: Applications to medical science Reviewed

    N Taniguchi, S Koyota, T Tsuda, W Wang, W Li, JH Ko, K Noda, M Takahashi, Y Ikeda, E Miyoshi, K Honke

    JOURNAL OF CLINICAL BIOCHEMISTRY AND NUTRITION   28 ( 3 )   217 - 232   2000

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  • Aldehyde reductase gene expression by lipid peroxidation end products, MDA and HNE Reviewed

    YH Koh, YS Park, M Takahashi, K Suzuki, N Taniguchi

    FREE RADICAL RESEARCH   33 ( 6 )   739 - 746   2000

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  • Overexpression of the aldose reductase gene induces apoptosis in pancreatic beta-cells by causing a redox imbalance Reviewed

    R Hamaoka, J Fujii, J Miyagawa, M Takahashi, M Kishimoto, M Moriwaki, K Yamamoto, Y Kajimoto, Y Yamasaki, T Hanafusa, Y Matsuzawa, N Taniguchi

    JOURNAL OF BIOCHEMISTRY   126 ( 1 )   41 - 47   1999.7

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  • Glycosyltransferases: cell surface remodeling and regulation of receptor tyrosine kinases-induced signaling Reviewed

    N Taniguchi, SK Jain, M Takahashi, JH Ko, K Sasai, E Miyoshi, Y Ikeda

    PURE AND APPLIED CHEMISTRY   71 ( 5 )   719 - 728   1999.5

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    DOI： 10.1351/pac199971050719

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  • Physiological relevance of aldehyde reductase and aldose reductase gene expression Reviewed

    J Fujii, M Takahashi, R Hamaoka, Y Kawasaki, N Miyazawa, N Taniguchi

    ENZYMOLOGY AND MOLECULAR BIOLOGY OF CARBONYL METABOLISM 7   463   419 - 426   1999

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  • A defect in the mitochondrial import of mutant Mn-superoxide dismutase produced in Sf21 cells Reviewed

    J Fujii, Y Ikeda, T Watanabe, Y Kawasaki, K Suzuki, C Fujii, M Takahashi, N Taniguchi

    JOURNAL OF BIOCHEMISTRY   124 ( 2 )   340 - 346   1998.8

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  • Selective induction of heparin-binding epidermal growth factor-like growth factor by methylglyoxal and 3-deoxyglucosone in rat aortic smooth muscle cells - The involvement of reactive oxygen species formation and a possible implication for atherogenesis in diabetes Reviewed

    WY Che, M Asahi, M Takahashi, H Kaneto, A Okado, S Higashiyama, N Taniguchi

    JOURNAL OF BIOLOGICAL CHEMISTRY   272 ( 29 )   18453 - 18459   1997.7

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    DOI： 10.1074/jbc.272.29.18453

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  • Immunoglobulin G is associated with surfactant protein A aggregate isolated from patients with pulmonary alveolar proteinosis Reviewed

    A Hattori, Y Kuroki, H Takahashi, H Sohma, T Akino

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE   155 ( 5 )   1785 - 1788   1997.5

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    DOI： 10.1164/ajrccm.155.5.9154892

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  • Molecular cloning and expression of amadoriase isoenzyme (fructosyl amine:oxygen oxidoreductase, EC 1.5.3) from Aspergillus fumigatus Reviewed

    M Takahashi, M Pischetsrieder, VM Monnier

    JOURNAL OF BIOLOGICAL CHEMISTRY   272 ( 19 )   12505 - 12507   1997.5

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    DOI： 10.1074/jbc.272.19.12505

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  • Isolation, purification, and characterization of amadoriase isoenzymes (fructosyl amine-oxygen oxidoreductase EC 1.5.3) from Aspergillus sp Reviewed

    M Takahashi, M Pischetsrieder, VM Monnier

    JOURNAL OF BIOLOGICAL CHEMISTRY   272 ( 6 )   3437 - 3443   1997.2

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    DOI： 10.1074/jbc.272.6.3437

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  • Glycation and inactivation of sorbitol dehydrogenase in normal and diabetic rats Reviewed

    A Hoshi, M Takahashi, J Fujii, T Myint, H Kaneto, K Suzuki, Y Yamasaki, T Kamada, N Taniguchi

    BIOCHEMICAL JOURNAL   318   119 - 123   1996.8

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  • Induction of apoptotic cell death by methylglyoxal and 3-deoxyglucosone in macrophage-derived cell lines Reviewed

    A Okado, Y Kawasaki, Y Hasuike, M Takahashi, T Teshima, J Fujii, N Taniguchi

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   225 ( 1 )   219 - 224   1996.8

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    DOI： 10.1006/bbrc.1996.1157

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  • Involvement of glycation and oxidative stress in diabetic macroangiopathy Reviewed

    N Taniguchi, H Kaneto, R Asahi, M Takahashi, WY Che, S Higashiyama, J Fujii, K Suzuki, Y Kayanoki

    DIABETES   45   S81 - S83   1996.7

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  • Instability of mutant Cu/Zn superoxide dismutase (Ala4Thr) associated with familial amyotrophic lateral sclerosis Reviewed

    R Nakano, T Inuzuka, K Kikugawa, H Takahashi, K Sakimura, J Fujii, N Taniguchi, S Tsuji

    NEUROSCIENCE LETTERS   211 ( 2 )   129 - 131   1996.6

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    DOI： 10.1016/0304-3940(96)12701-4

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  • Induction of aldose reductase gene expression in LEC rats during the development of the hereditary hepatitis and hepatoma Reviewed

    M Takahashi, A Hoshi, J Fujii, E Miyoshi, T Kasahara, K Suzuki, K Aozasa, N Taniguchi

    JAPANESE JOURNAL OF CANCER RESEARCH   87 ( 4 )   337 - 341   1996.4

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  • FRAGMENTATION OF CERULOPLASMIN FOLLOWING NONENZYMATIC GLYCATION REACTION Reviewed

    KN ISLAM, M TAKAHASHI, S HIGASHIYAMA, T MYINT, N UOZUMI, Y KAYANOKI, H KANETO, H KOSAKA, N TANIGUCHI

    JOURNAL OF BIOCHEMISTRY   118 ( 5 )   1054 - 1060   1995.11

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  • ELEVATION OF ALDOSE REDUCTASE GENE-EXPRESSION IN RAT PRIMARY HEPATOMA AND HEPATOMA-CELL LINES - IMPLICATION IN DETOXIFICATION OF CYTOTOXIC ALDEHYDES Reviewed

    M TAKAHASHI, J FUJII, E MIYOSHI, A HOSHI, N TANIGUCHI

    INTERNATIONAL JOURNAL OF CANCER   62 ( 6 )   749 - 754   1995.9

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    DOI： 10.1002/ijc.2910620617

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  • IN-VIVO GLYCATION OF ALDEHYDE REDUCTASE, A MAJOR 3-DEOXYGLUCOSONE REDUCING ENZYME - IDENTIFICATION OF GLYCATION SITES Reviewed

    M TAKAHASHI, YB LU, T MYINT, J FUJII, Y WADA, N TANIGUCHI

    BIOCHEMISTRY   34 ( 4 )   1433 - 1438   1995.1

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    DOI： 10.1021/bi00004a038

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  • GLYCATION OF HUMAN BETA-(2)-MICROGLOBULIN IN PATIENTS WITH HEMODIALYSIS-ASSOCIATED AMYLOIDOSIS - IDENTIFICATION OF THE GLYCATED SITES Reviewed

    T MIYATA, R INAGI, Y WADA, Y UEDA, Y IIDA, M TAKAHASHI, N TANIGUCHI, K MAEDA

    BIOCHEMISTRY   33 ( 40 )   12215 - 12221   1994.10

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    DOI： 10.1021/bi00206a026

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  • Selective suppression of IgG2a subclass in LEC rats during development. Reviewed

    Ikeda Y, Sugiyama T, Takahashi M, Taniguchi N

    Biochimica et biophysica acta   1200   277 - 280   1994.8

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  • A NOVEL MUTATION IN CU/ZN SUPEROXIDE-DISMUTASE GENE IN JAPANESE FAMILIAL AMYOTROPHIC-LATERAL-SCLEROSIS Reviewed

    R NAKANO, S SATO, T INUZUKA, K SAKIMURA, M MISHINA, H TAKAHASHI, F IKUTA, Y HONMA, J FUJII, N TANIGUCHI, S TSUJI

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   200 ( 2 )   695 - 703   1994.4

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    DOI： 10.1006/bbrc.1994.1506

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  • IDENTITY OF A MAJOR 3-DEOXYGLUCOSONE-REDUCING ENZYME WITH ALDEHYDE REDUCTASE IN RAT-LIVER ESTABLISHED BY AMINO-ACID SEQUENCING AND CDNA EXPRESSION Reviewed

    M TAKAHASHI, J FUJII, T TESHIMA, K SUZUKI, T SHIBA, N TANIGUCHI

    GENE   127 ( 2 )   249 - 253   1993.5

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  • Segregated Microstructure in Sputtered Co-Cr Films by Selective Chemical Etching Reviewed

    M. Takahashi, Y. Maeda, M. Asahi

    IEEE Translation Journal on Magnetics in Japan   3 ( 7 )   515 - 516   1988

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    DOI： 10.1109/TJMJ.1988.4563771

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  • CINC-2 and miR-199a-5p in exosomes secreted by transplanted Thy1+ cells activate hepatocytic progenitor cell growth in rat liver regeneration

    Norihisa Ichinohe, Naoki Tanimizu, Keisuke Ishigami, Yusuke Yoshioka, Naoki Fujitani, Takahiro Ochiya, Motoko Takahashi, Toshihiro Mitaka

    Research Square   2023.1

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    Abstract

    Background Small hepatocyte-like progenitor cells (SHPCs) are hepatocytic progenitor cells that transiently form clusters in rat livers treated with retrorsine and with 70% partial hepatectomy (PH). We previously reported that transplantation of Thy1<sup>+</sup> cells derived from d-galactosamine-treated livers promotes SHPC expansion, resulting in the acceleration of liver regeneration. Extracellular vesicles (EVs) produced by Thy1<sup>+</sup> cells act on sinusoidal endothelial cells (SECs) and Kupffer cells to secrete IL17B and IL25, respectively, resulting in SHPC activation through IL17 receptor B (RB) signaling. Our aim is to identify factors in Thy1-EVs that activate IL17RB signaling.Methods Thy1<sup>+</sup> cells isolated from rats with d-galactosamine-induced liver injury were cultured for one week. Although some liver stem/progenitor cells proliferated into colonies, others maintained as mesenchymal cells (MCs). Thy1-MCs or Thy1-liver stem/progenitor cells were transplanted into retrorsine/PH-treated livers to examine their effects on SHPCs. SHs isolated from adult rat livers were used to validate factors regulating growth induction.Results The number and size of SHPCs remarkably increased in livers transplanted with Thy1-MCs. Comprehensive analysis of Thy1-MC-EVs revealed that miR-199a-5p, CINC-2, and MCP-1 are candidates for stimulating SHPC growth. Administration of the miR-199a-5p mimic, and not CINC-2, promoted SH growth. SECs treated with CINC-2 induced IL17b expression and their conditioned medium promoted SH growth.Conclusion Thy1-MC transplantation may accelerate liver regeneration due to SHPCs expansion, which is stimulated by CINC-2/IL17RB signaling and miR-199a-5p.

    Other Link:： https://www.researchsquare.com/article/rs-2087658/v1.html

    DOI： 10.21203/rs.3.rs-2087658/v1

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  • Site-specific Analysis of N-glycans of Receptor Tyrosine Kinases

    高橋素子, 藤谷直樹, 上原康昭, 長谷川喜弘

    Trends in Glycoscience and Glycotechnology (Web)   35 ( 206 )   2023

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  • Structural and functional analysis of N-glycans of growth factor receptors

    高橋素子, 岡本弘美, 藤谷直樹, 上原康昭, 橋本宇吉郎, 長谷川喜弘

    日本糖質学会年会要旨集   42nd   2023

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  • Structural and functional analysis of N-glycans of hepatocyte growth factor receptor MET

    高橋素子, 齋藤淳, 長谷川喜弘, 藤谷直樹, 有木茂, 上原康昭, 松本邦夫

    日本糖質学会年会要旨集   41st   2022

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  • 臨床応用を目指した肺胞微石症の基礎および治療法の検討

    齋藤充史, 齋藤充史, 齋藤淳, 齋藤淳, 藤谷直樹, 有木茂, 高橋素子, 高橋弘毅

    日本呼吸器学会誌(Web)   8   2019

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  • ErbB受容体の糖鎖の構造と機能

    高橋素子, 藤谷直樹, 和田芳直, 加藤公児, YAO Min

    日本糖質学会年会要旨集   38th   2019

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  • 細胞グライコミクスから部位特異的グライコミクスへ:生物学的機能を明らかにするための部位特異的なN結合型糖鎖の構造解析

    藤谷直樹, 高橋素子

    日本分子生物学会年会プログラム・要旨集(Web)   42nd   2019

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  • 肺サーファクタントタンパク質Dは変異型EGFRの活性化を阻害し、肺腺がんの進展を抑制する

    長谷川 喜弘, 梅田 泰淳, 大塚 満雄, 有木 茂, 高宮 里奈, 齋藤 充史, 高橋 弘毅, 黒木 由夫, 高橋 素子

    生命科学系学会合同年次大会   2017年度   [1P - 0948]   2017.12

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  • タバコ煙中のアクロレインが肺サーファクタントタンパク質A(SP‐A)に及ぼす影響

    高宮里奈, 内田浩二, 内田浩二, 柴田貴広, 前野敏孝, 加藤雅樹, 山口芳樹, 有木茂, 長谷川喜弘, 齋藤充史, 高橋素子, 黒木由夫

    日本糖質学会年会要旨集   36th   84   2017.7

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  • SP‐DによるEGFR制御機構

    長谷川喜弘, 長谷川喜弘, 高橋素子, 高橋弘毅

    Bio Clinica   6 ( 1 )   130‐134 - 134   2017.3

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  • SP-Dによる変異型EGFR肺がんの制御機構

    長谷川 喜弘, 梅田 泰淳, 大塚 満雄, 有木 茂, 高宮 里奈, 齋藤 充史, 黒沼 幸治, 千葉 弘文, 高橋 弘毅, 黒木 由夫, 高橋 素子

    分子呼吸器病   21 ( 1 )   80 - 83   2017.3

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  • SP-Dによる変異型EGFR肺がんの制御機構

    長谷川 喜弘, 梅田 泰淳, 大塚 満雄, 有木 茂, 高宮 里奈, 齋藤 充史, 黒沼 幸治, 千葉 弘文, 高橋 弘毅, 黒木 由夫, 高橋 素子

    分子呼吸器病   21 ( 1 )   80 - 83   2017.3

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  • 糖鎖改変・可溶型EGFRによるEGFシグナル抑制作用のメカニズム

    高橋素子, 長谷川喜弘, 加藤公児, 姚閔, 和田芳直, 有木茂, 高宮里奈, 齋藤充史, 黒木由夫

    日本生化学会大会(Web)   89th   ROMBUNNO.1T08‐01(1P‐042) (WEB ONLY) - 01(1P   2016.9

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  • 肺サーファクタント蛋白質SP‐Dの肺がんに対する新たな役割

    長谷川喜弘, 長谷川喜弘, 高橋素子, 高橋弘毅

    月刊メディカル・サイエンス・ダイジェスト   42 ( 9 )   398‐402 - 402   2016.8

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  • EGFRのN‐型糖鎖の機能

    高橋素子, 長谷川喜弘, 和田芳直, 加藤公児, YAO Min, 有木茂, 高宮里奈, 齋藤充史, 黒木由夫

    日本糖質学会年会要旨集   35th   138   2016.8

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  • SP-AおよびSP-A由来ペプチドはヒトβ-デフェンシン3による肥満細胞の遊走を抑制する

    有木 茂, 上原 康昭, 村田 雅樹, 高宮 里奈, 長谷川 喜弘, 斎藤 充史, 千葉 弘文, 黒沼 幸治, 高橋 素子, 高橋 弘毅, 黒木 由夫

    分子呼吸器病   20 ( 1 )   120 - 123   2016.3

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  • SP-DによるEGFR遺伝子変異陽性肺腺癌における制御機構

    梅田泰淳, 長谷川喜弘, 長谷川喜弘, 大塚満雄, 黒沼幸治, 高橋素子, 高橋弘毅

    日本肺サーファクタント・界面医学会学術研究会プログラム・抄録集   52nd   2016

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  • 糖鎖改変・可溶型ErbB3による抗腫瘍作用の分子メカニズム

    高橋素子, 加藤公児, 姚閔, 和田芳直, 田尻道子, 長谷川喜弘, 高宮里奈, 有木茂, 黒木由夫

    日本生化学会大会(Web)   88th   1TTOKU04(1P0263) (WEB ONLY) - 04(1P0263)]   2015.12

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  • 膀胱におけるサーファクタント蛋白質Aの発現と尿路病原性大腸菌に対する感染防御機構

    橋本 次朗, 高橋 聡, 舛森 直哉, 有木 茂, 高宮 里奈, 高橋 素子, 黒木 由夫, 上原 康昭, 長谷川 善弘

    泌尿器外科   28 ( 5 )   1001 - 1002   2015.5

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  • 膀胱におけるサーファクタント蛋白質Aの発現と尿路病原性大腸菌に対する感染防御機構

    橋本 次朗, 有木 茂, 高宮 里奈, 高橋 素子, 上原 康昭, 長谷川 善弘, 高橋 聡, 黒木 由夫, 舛森 直哉

    日本泌尿器科学会総会   103回   742 - 742   2015.4

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  • 膀胱におけるサーファクタント蛋白質Aの発現と尿路病原性大腸菌に対する感染防御機構

    橋本 次朗, 高橋 聡, 上原 康昭, 長谷川 喜弘, 舛森 直哉, 有木 茂, 高宮 里奈, 高橋 素子, 黒木 由雄

    日本化学療法学会雑誌   63 ( 2 )   252 - 252   2015.3

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  • 肺サーファクタント蛋白質のEGFシグナル制御を介した抗腫瘍作用

    長谷川 喜弘, 高橋 素子, 有木 茂, 高宮 里奈, 上原 康昭, 橋本 次朗, 和田 芳直, 高橋 弘毅, 黒木 由夫

    分子呼吸器病   19 ( 1 )   107 - 111   2015.3

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  • SP-AとSP-DによるEGFシグナル制御を介した抗腫瘍作用

    長谷川 喜弘, 高橋 素子, 有木 茂, 高宮 里奈, 上原 康昭, 橋本 次朗, 和田 芳直, 高橋 弘毅, 黒木 由夫

    日本呼吸器学会誌   4 ( 増刊 )   173 - 173   2015.3

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  • 【肺癌Up-To-Date】 基礎医学とのダイアローグ 肺サーファクタントタンパク質SP-Dによる肺癌の進展の抑制

    高橋 素子, 長谷川 喜弘, 黒木 由夫

    THE LUNG-perspectives   23 ( 1 )   65 - 69   2015.2

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  • ErbBシグナルを介したがんにおける酸素応答機構の解明

    高宮里奈, 高橋素子, 佐久間裕司, 長谷川喜弘, 有木茂, 鈴木拓, 黒木由夫

    日本酸化ストレス学会学術集会プログラム・抄録集   68th   2015

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  • EGFRのドメインIIIの糖鎖による機能制御

    高橋素子, 長谷川喜弘, 高宮里奈, 和田芳直, 田尻道子, 浅川大樹, 有木茂, 黒木由夫

    日本糖質学会年会要旨集   34th   2015

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  • N-glycan deletion mutant of soluble ErbB3 protein attenuates heregulin-induced tumor progression by blockade of HIF-1 pathway

    Rina Takamiya, Motoko Takahashi, Yoshihiro Hasegawa, Yasuaki Uehara, Jiro Hashimoto, Shigeru Ariki, Yoshio Kuroki

    GLYCOBIOLOGY   24 ( 11 )   1200 - 1200   2014.11

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  • Signaling-inhibitory effects of sErbB3 is enhanced by single N-glycan deletion

    Motoko Takahashi, Yoshihiro Hasegawa, Yoshitaka Ikeda, Yoshinao Wada, Michiko Tajiri, Shigeru Ariki, Rina Takamiya, Yoshiki Yamaguchi, Naoyuki Taniguchi, Yoshio Kuroki

    GLYCOBIOLOGY   24 ( 11 )   1149 - 1149   2014.11

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  • タンパク質の物性を制御する糖鎖 N型糖鎖によるErbB受容体の機能制御メカニズム

    高橋 素子, 黒木 由夫

    日本生化学会大会プログラム・講演要旨集   87回   [3S05p - 2]   2014.10

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  • 肺コレクチンの単球機能への影響

    高宮 里奈, 村田 雅樹, 上原 康昭, 有木 茂, 長谷川 喜弘, 橋本 次朗, 高橋 素子, 澤田 典均, 黒木 由夫

    日本生化学会大会プログラム・講演要旨集   87回   [2T16a - 01]   2014.10

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  • 肺サーファクタント蛋白質AとDによるEGFシグナルの抑制作用

    長谷川 喜弘, 高橋 素子, 有木 茂, 高宮 里奈, 上原 康昭, 橋本 次朗, 浅川 大樹, 田尻 道子, 和田 芳直, 高橋 弘毅, 黒木 由夫

    日本生化学会大会プログラム・講演要旨集   87回   [2T15a - 14]   2014.10

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  • 【呼吸器感染症研究における新しい展開】 肺サーファクタントの感染・炎症防御における役割

    高橋 素子, 有木 茂, 黒木 由夫

    呼吸器内科   26 ( 1 )   33 - 41   2014.7

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  • Regulation Of Tumor Microenvironment By Tumor Associated Sialyl-Tn Antigen On Integrin

    R. Takamiya, S. Takamatsu, T. Angata, M. Takahashi, Y. Kuroki, N. Taniguchi, K. Ohtsubo

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE   189   2014

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  • Surfactant Protein A-Derived Peptide Decreases Cytotoxicity Of Human beta-Defensin 3 Without Attenuating Antimicrobial Activity

    Y. Uehara, S. Ariki, M. Takahashi, R. Takamiya, Y. Hasegawa, H. Takahashi, Y. Kuroki

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE   189   2014

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  • Surfactant Proteins A And D Suppress Lung Cancer Progression By Downregulation Of Egf Signaling

    Y. Hasegawa, M. Takahashi, S. Ariki, R. Takamiya, Y. Uehara, J. Hashimoto, H. Takahashi, Y. Kuroki

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE   189   2014

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  • サーファクタント蛋白質による尿路病原性大腸菌感染防御

    栗村 雄一郎, 上原 央久, 橋本 次朗, 高橋 聡, 舛森 直哉, 有木 茂, 西谷 千明, 高橋 素子, 黒木 由夫, 塚本 泰司

    泌尿器外科   26 ( 12 )   1858 - 1858   2013.12

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  • コレクチンによる自然免疫機構

    黒木 由夫, 有木 茂, 西谷 千明, 高橋 素子

    緑膿菌感染症研究会講演記録   47回   1 - 6   2013.12

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  • SURFACTANT PROTEIN A-DERIVED PEPTIDE PROTECTS LUNG EPITHELIAL CELLS FROM CYTOTOXIC ACTIVITY OF HUMAN beta-DEFENSIN 3

    Yasuaki Uehara, Shigeru Ariki, Motoko Takahashi, Rina Takamiya, Yoshihiro Hasegawa, Hiroki Takahashi, Yoshio Kuroki

    RESPIROLOGY   18   102 - 102   2013.11

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  • 【生体防御能の異常・免疫障害で見られる感染症の特徴とメカニズム】 肺コレクチンの欠損による易感染性と肺胞構造の異常

    高橋 素子, 黒木 由夫

    化学療法の領域   29 ( 12 )   2435 - 2443   2013.11

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  • 可溶型ErbB3糖鎖欠損変異体とラパチニブのヘレグリンシグナル抑制作用における相乗効果

    高橋 素子, 長谷川 喜弘, 有木 茂, 高宮 里奈, 和田 芳直, 田尻 道子, 黒木 由夫

    日本生化学会大会プログラム・講演要旨集   86回   2P - 004   2013.9

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  • 肺サーファクタント蛋白質A由来ペプチドはヒトβディフェンシン3の細胞傷害を抑制する

    上原 康昭, 有木 茂, 高橋 素子, 高宮 里奈, 長谷川 喜弘, 橋本 次郎, 高橋 弘毅, 黒木 由夫

    日本生化学会大会プログラム・講演要旨集   86回   1T18p - 05   2013.9

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  • 肺コレクチンによるEGFシグナルの制御機構

    長谷川 喜弘, 高橋 素子, 有木 茂, 高宮 里奈, 上原 康昭, 橋本 次郎, 高橋 弘毅, 黒木 由夫

    日本生化学会大会プログラム・講演要旨集   86回   1T10p - 04   2013.9

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  • がん関連糖鎖シアリルTn糖鎖抗原発現によるインテグリンを介したがん微小環境制御機構

    高宮 里奈, 大坪 和明, 高松 真二, 安形 高志, 高橋 素子, 黒木 由夫, 谷口 直之

    日本生化学会大会プログラム・講演要旨集   86回   1T10p - 02   2013.9

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  • AKR1AならびにxCT遺伝子改変マウスを用いた低分子量レドックス分子のクロストークに関する研究

    李 在勇, 倉橋 敏裕, 権 明秀, 高橋 素子, 大槻 倫之, 伊藤 純一, 松岡 悠太, 山田 健一, 宮田 哲, 佐藤 英世, 藤井 順逸

    日本生化学会大会プログラム・講演要旨集   86回   3P - 176   2013.9

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  • 肺サーファクタント蛋白質A由来ペプチドはヒトβディフェンシン3の細胞傷害を抑制する

    上原 康昭, 有木 茂, 高橋 素子, 高宮 里奈, 長谷川 喜弘, 橋本 次郎, 高橋 弘毅, 黒木 由夫

    日本生化学会大会プログラム・講演要旨集   86回   2P - 469   2013.9

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  • 遺伝子改変マウスおよびマウス胎仔線維芽細胞を用いたアルデヒド還元酵素AKR1Aの機能解析

    権 明秀, 大槻 倫之, 金野 祐, 角田 智志, 倉橋 敏裕, 伊藤 純一, 高橋 素子, 宮田 哲, 藤井 順逸

    山形医学   31 ( 2 )   55 - 55   2013.8

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  • コレクチンによる自然免疫機構

    黒木 由夫, 有木 茂, 高橋 素子

    Therapeutic Research   34 ( 6 )   766 - 768   2013.6

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  • Aldehyde reductase欠損によるアスコルビン酸合成障害のPentobarbita代謝に与える影響

    伊藤 純一, 大槻 倫之, 高橋 素子, 権 明秀, 金野 祐, 角田 智志, 倉橋 敏裕, 張 旭紅, 宮田 哲, 藤井 順逸

    日本生化学会大会プログラム・講演要旨集   85回   2P - 334   2012.12

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  • サーファクタント蛋白質D(SP-D)は、膀胱上皮への尿路病原性大腸菌感染を防御する 膀胱に発現するSP-Dの生理的役割の解明(Surfactant protein D protects the bladder urothelium against uropathogenic Escherichia coli infection: A possible function of SP-D expressed in the bladder)

    西谷 千明, 栗村 雄一郎, 有木 茂, 齋藤 充史, 長谷川 喜弘, 高橋 素子, 橋本 次朗, 高橋 聡, 塚本 泰司, 黒木 由夫

    日本生化学会大会プログラム・講演要旨集   85回   3P - 843   2012.12

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  • Aldehyde reductase(AKR1A)欠損によるアスコルビン酸合成障害の血液系に与える影響

    金野 祐, 大槻 倫之, 権 明秀, 角田 智志, 伊藤 純一, 倉橋 敏裕, 松岡 悠太, 山崎 俊栄, 山田 健一, 宮田 智, 高橋 素子, 藤井 順逸

    日本生化学会大会プログラム・講演要旨集   85回   3P - 343   2012.12

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  • 可溶型ErbB受容体によるヘレグリンシグナル抑制機構

    高橋 素子, 長谷川 喜弘, 西谷 千明, 有木 茂, 和田 芳直, 田尻 道子, 黒木 由夫

    日本生化学会大会プログラム・講演要旨集   85回   3T25 - 01   2012.12

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  • 肺コレクチンによるEGFシグナルの制御機構

    長谷川 喜弘, 高橋 素子, 上原 康昭, 有木 茂, 西谷 千明, 高橋 弘毅, 黒木 由夫

    日本生化学会大会プログラム・講演要旨集   85回   2P - 783   2012.12

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  • 肝臓の解毒反応におけるアルデヒド還元酵素の役割の遺伝子改変マウスを用いた解明

    伊藤 純一, 大槻 倫之, 高橋 素子, 権 明秀, 金野 祐, 角田 智, 倉橋 敏裕, 張 旭紅, 宮田 哲, 藤井 順逸

    肝臓   53 ( Suppl.2 )   A699 - A699   2012.9

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  • アスコルビン酸合成異常を示すAldehyde reductase(AKR1A1)欠損マウスの表現型解析

    大槻 倫之, 伊藤 純一, 張 旭紅, 高橋 素子, 西田 隼人, 倉橋 敏裕, 権 明秀, 角田 智志, 金野 祐, 宮田 哲, 藤井 順逸

    山形医学   30 ( 2 )   81 - 81   2012.8

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  • マウス卵初期発生過程におけるアスコルビン酸(VC)含量とVC合成系・取込み系遺伝子の発現

    星野 由貴, 樋口 謙太, 梅田 彩, 高橋 素子, 宮田 哲, 吉田 康一, 藤井 順逸, 木村 直子

    The Journal of Reproduction and Development   58 ( Suppl. )   j186 - j186   2012.8

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  • Innate immune system by pulmonary collectins

    Yoshio Kuroki, Shigeru Ariki, Chiaki Nishitani, Motoko Takahashi

    Japanese Journal of Clinical Chemistry   41 ( 2 )   159 - 165   2012.4

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  • 肺コレクチンによる自然免疫機構

    黒木 由夫, 有木 茂, 西谷 千明, 高橋 素子

    臨床化学   41 ( 2 )   159 - 165   2012.4

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  • 非結核性抗酸菌に対するSP-A・SP-Dの感染防御機構

    有木 茂, 齋藤 充史, 西谷 千明, 高橋 素子, 黒木 由夫

    分子呼吸器病   16 ( 1 )   121 - 124   2012.3

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  • 酸化肺サーファクタントリン脂質によるLPS惹起炎症応答抑制機構

    西谷 千明, 有木 茂, 高橋 素子, 栗村 雄一郎, 斎藤 充史, 長谷川 喜弘, 清水 健之, 黒木 由夫

    エンドトキシン・自然免疫研究   14   43 - 45   2011.11

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  • レジオネラ菌に対する肺コレクチンの生体防御機構

    齋藤 充史, 有木 茂, 西谷 千明, 高橋 素子, 高橋 弘毅, 黒木 由夫

    エンドトキシン・自然免疫研究   14   79 - 82   2011.11

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  • 非結核性抗酸菌感染に対する肺コレクチンの生体防御機構

    有木 茂, 齋藤 充史, 西谷 千明, 高橋 素子, 黒木 由夫

    エンドトキシン・自然免疫研究   14   83 - 85   2011.11

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  • 肺コレクチンはレジオネラ感染により誘導されるオートファジーを抑制する

    齋藤 充史, 有木 茂, 長谷川 喜弘, 栗村 雄一郎, 西谷 千明, 高橋 素子, 高橋 弘毅, 黒木 由夫

    日本肺サーファクタント・界面医学会雑誌   42   32 - 32   2011.10

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  • 糖鎖改変・可溶型ErbB3によるヘレギュリンシグナル抑制効果(Inhibition of heregulin signaling by N-glycan deleted soluble ErbB3)

    高橋 素子, 和田 芳直, 田尻 道子, 山口 芳樹, 西谷 千明, 有木 茂, 谷口 直之, 黒木 由夫

    日本生化学会大会プログラム・講演要旨集   84回   2T8a - 4   2011.9

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  • 尿路病原性大腸菌感染に対するサーファクタント蛋白質の防御的役割

    西谷 千明, 栗村 雄一郎, 有木 茂, 高橋 素子, 齋藤 充史, 長谷川 喜弘, 橋本 次朗, 高橋 聡, 相馬 仁, 塚本 泰司, 黒木 由夫

    日本生化学会大会プログラム・講演要旨集   84回   4T16a - 5   2011.9

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  • サーファクタント蛋白質Aは肺上皮細胞をヒトβ-defensin 3の細胞毒性から保護する(Surfactant protein A protects lung epithelial cells from cytotoxic activity of human beta-defensin 3)

    齋藤 充史, 有木 茂, 長谷川 喜弘, 西谷 千明, 高橋 素子, 相馬 仁, 高橋 弘毅, 黒木 由夫

    日本生化学会大会プログラム・講演要旨集   84回   4T8a - 10   2011.9

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  • アルデヒド還元酵素(ALR)遺伝子改変マウスを用いたペントバルビタール解毒障害機序の解明

    大槻 倫之, 伊藤 純一, 高橋 素子, 西田 隼人, 金野 祐, 角田 智志, 倉橋 敏裕, 張 旭紅, 宮田 哲, 藤井 順逸

    山形医学   29 ( 2 )   79 - 79   2011.8

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  • マウス卵発生過程におけるアスコルビン酸(VC)合成系遺伝子の発現とその役割

    樋口 謙太, 酒出 はるな, 高橋 素子, 宮田 哲, 藤井 順逸, 木村 直子

    The Journal of Reproduction and Development   57 ( Suppl. )   j149 - j149   2011.8

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    DOI： 10.14882/jrds.104.0.1016.0

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  • SURFACTANT PROTEINS A AND D INHIBIT UROPATHOGENIC ESCHERICHIA COLI BINDING TO UROTHELIAL CELLS

    Yuichiro Kurimura, Teruhisa Uehara, Kohji Ichihara, Jiro Hashimoto, Satoshi Takahashi, Shigeru Ariki, Chiaki Nishitani, Motoko Takahashi, Yoshio Kuroki, Taiji Tsukamoto

    JOURNAL OF UROLOGY   185 ( 4 )   E546 - E546   2011.4

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  • APP-078 尿路におけるサーファクタント蛋白質(SP-A、SP-D)の感染防御 : 尿路病原性大腸菌の尿路上皮への接着阻害(総会賞応募ポスター,第99回日本泌尿器科学会総会)

    栗村 雄一郎, 西谷 千明, 橋本 次朗, 高橋 聡, 有木 茂, 高橋 素子, 黒木 由夫, 塚本 泰司

    日本泌尿器科學會雜誌   102 ( 2 )   331 - 331   2011.3

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    DOI： 10.5980/jpnjurol.102.331_2

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  • 尿路におけるサーファクタント蛋白質(SP-A、SP-D)の感染防御 尿路病原性大腸菌の尿路上皮への接着阻害

    栗村 雄一郎, 西谷 千明, 橋本 次朗, 高橋 聡, 有木 茂, 高橋 素子, 黒木 由夫, 塚本 泰司

    日本泌尿器科学会雑誌   102 ( 2 )   331 - 331   2011.3

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    DOI： 10.5980/jpnjurol.102.331_2

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  • Oxidized Surfactant Lipids And Oxidized PAPC Attenuate LPS-Induced Inflammatory Responses By Different Mechanisms

    C. Nishitani, S. Ariki, M. Takahashi, Y. Kurimura, A. Saito, T. Shimizu, Y. Kuroki

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE   183   2011

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  • Pulmonary Collectins Attenuate Autophagy Induced By L. Pneumophila Infection

    A. Saito, S. Ariki, C. Nishitani, M. Takahashi, H. Takahashi, Y. Kuroki

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE   183   2011

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  • 肺コレクチンはLegionella pneumophila感染により誘導されるオートファジーを阻害する(Pulmonary collectins inhibit the autophagy induced by Legionella pneumophila infection)

    齋藤 充史, 有木 茂, 長谷川 喜弘, 栗村 雄一郎, 西谷 千明, 高橋 素子, 高橋 弘毅, 黒木 由夫

    日本生化学会大会・日本分子生物学会年会合同大会講演要旨集   83回・33回   4P - 0008   2010.12

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  • 肺コレクチンはM. aviumに結合して凝集させ、その増殖を抑制する(Pulmonary collectins bind and agglutinate M. avium and attenuate its growth)

    有木 茂, 賀佐 伸省, 小島 隆, 斎藤 充史, 西谷 千明, 高橋 素子, 清水 健之, 栗村 雄一郎, 澤田 典均, 藤井 暢弘, 黒木 由夫

    日本生化学会大会・日本分子生物学会年会合同大会講演要旨集   83回・33回   4T6 - 4   2010.12

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  • 酸化肺サーファクタントリン脂質によるLPS惹起炎症性細胞応答抑制機構の解明(Oxidized surfactant lipids and oxidized PAPC inhibit LPS-induced inflammatory responses by different mechanisms)

    西谷 千明, 有木 茂, 高橋 素子, 清水 健之, 栗村 雄一郎, 齋藤 充史, 長谷川 喜弘, 黒木 由夫

    日本生化学会大会・日本分子生物学会年会合同大会講演要旨集   83回・33回   3P - 0128   2010.12

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  • コレクチンの免疫グロブリンに対する結合性の解析(Analysis of interactions between collectins and immunoglobulins)

    清水 健之, 高橋 素子, 西谷 千明, 有木 茂, 黒木 由夫

    日本生化学会大会・日本分子生物学会年会合同大会講演要旨集   83回・33回   4P - 0009   2010.12

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  • マウスのアスコルビン酸生合成におけるアルデヒドレダクターゼの関与(The involvement of aldehyde reductase in biosynthesis of ascorbic acid in mice)

    高橋 素子, 藤井 順逸, 荒木 素子, 井内 陽子, 曽我 朋義, 宮田 哲, 谷口 直之, 黒木 由夫

    日本生化学会大会・日本分子生物学会年会合同大会講演要旨集   83回・33回   4P - 0341   2010.12

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  • 肺における細胞内輸送機能と病態生理 SP-DはLPSとその受容体に対する結合を変化させることによりLPS惹起炎症反応を抑制する

    山添 雅己, 西谷 千明, 高橋 素子, 加藤 剛志, 有木 茂, 清水 健之, 光澤 博昭, 澤田 格, 高橋 弘毅, 黒木 由夫

    分子呼吸器病   14 ( 1 )   101 - 105   2010.1

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  • マウスアスコルビン酸合成におけるアルデヒドレダクターゼの役割(The role of aldehyde reductase in biosynthesis of ascorbic acid in mice)

    高橋 素子, 井内 陽子, 宮田 哲, 錦見 盛光, 有木 茂, 谷口 直之, 黒木 由夫

    日本生化学会大会プログラム・講演要旨集   82回   2T6p - 15   2009.9

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  • 非定型抗酸菌に対する肺コレクチンの生体防御機構

    有木 茂, 澤田 格, 藤井 暢弘, 賀佐 伸省, 西谷 千明, 清水 健之, 山添 雅己, 高橋 素子, 黒木 由夫

    日本生化学会大会プログラム・講演要旨集   82回   4T20p - 11   2009.9

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  • 肺サーファクタントリン脂質の酸化によるLPS惹起炎症性細胞応答の抑制

    西谷 千明, 有木 茂, 清水 健之, 高橋 素子, 光澤 博昭, 黒木 由夫

    日本生化学会大会プログラム・講演要旨集   82回   4T5p - 7   2009.9

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  • Pulmonary Surfactant Protein D Inhibits Lipopolysaccharide (LPS)-Induced Inflammatory Cell Responses by Altering LPS Binding to Its Receptors

    Chiaki Nishitani, Masami Yamazoe, Motoko Takahashi, Tsuyoshi Katoh, Shigeru Ariki, Takeyuki Shimizu, Mitsuzawa Hiroaki, Kaku Sawada, Dennis R. Voelker, Hiroki Takahashi, Yoshio Kuroki

    FASEB JOURNAL   23   2009.4

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  • Roles of pulmonary collectins in host defense against Legionella pneumophila infection

    Shigeru Ariki, Kaku Sawada, Masami Yamazoe, Chiaki Nishitani, Takeyuki Shimizu, Motoko Takahashi, Shin-ichi Yokota, Nobuhiro Fujii, Hiroki Takahashi, Yoshio Kuroki

    FASEB JOURNAL   23   2009.4

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  • 肺胞上皮細胞に対する内的、外的諸分子の役割と病態生理 肺コレクチンによるレジオネラ菌の増殖抑制

    澤田 格, 有木 茂, 山添 雅己, 西谷 千明, 清水 健之, 高橋 素子, 横田 伸一, 藤井 暢弘, 高橋 弘毅, 黒木 由夫

    分子呼吸器病   13 ( 1 )   117 - 119   2009.1

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  • 肺コレクチンはレジオネラ菌に対して抗菌作用を有する(Pulmonary collectins exhibit anti-microbial activity against Legionella pneumophila)

    澤田 格, 有木 茂, 山添 雅己, 西谷 千明, 清水 健之, 高橋 素子, 横田 伸一, 藤井 暢弘, 高橋 弘毅, 黒木 由夫

    日本生化学会大会・日本分子生物学会年会合同大会講演要旨集   81回・31回   4T8 - 4   2008.11

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  • Human Pulmonary Surfactant Protein D Binds to MD-2

    NIE Xiaomeng, NISHITANI ONO Chiaki, YAMAZOE Masami, SHIMIZU Takeyuki, MITSUZAWA Hiroaki, SAWADA Kaku, TAKAHASHI Motoko, TAKAHASHI Hiroki, KUROKI Yoshio

    39   38 - 38   2008.10

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  • 【糖鎖情報の独自性と普遍性】 細胞膜における糖鎖複合体の構造と機能 受容体としての糖鎖、受容体との相互作用 受容体機能におけるコアフコースの重要性

    高橋 素子, 三善 英知, 顧 建国, 谷口 直之

    蛋白質・核酸・酵素   53 ( 12 )   1502 - 1507   2008.9

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  • The importance of core fucose in receptor function

    Protein, nucleic acid and enzyme   53 ( 12 )   1502 - 1507   2008.9

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  • 肺サーファクタント蛋白質Dによるリポ多糖惹起炎症反応の抑制

    山添 雅己, 有木 茂, 澤田 格, 西谷 千明, 清水 健之, 高橋 素子, 高橋 弘毅, 黒木 由夫

    補体シンポジウム講演集   45   196 - 197   2008.7

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  • TLR4の細胞表面発現におけるMD-2の重要性

    西谷 千明, 高橋 素子, 光澤 博昭, 清水 健之, 有木 茂, 松嶋 範男, 黒木 由夫

    補体シンポジウム講演集   45   195 - 195   2008.7

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  • レジオネラ菌に対する肺コレクチンの増殖抑制作用

    澤田 格, 有木 茂, 山添 雅己, 西谷 千明, 清水 健之, 高橋 素子, 横田 伸一, 藤井 暢弘, 高橋 弘毅, 黒木 由夫

    補体シンポジウム講演集   45   108 - 108   2008.7

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  • 肺コレクチンは非定型抗酸菌に結合し菌体凝集を惹起する

    有木 茂, 澤田 格, 賀佐 伸省, 藤井 暢弘, 山添 雅己, 清水 健之, 西谷 千明, 高橋 素子, 黒木 由夫

    補体シンポジウム講演集   45   198 - 198   2008.7

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  • 肺サーファクタントプロテインDは肺胞マクロファージにおいてlipopolysaccharide刺激に対する炎症反応を抑制する(Pulmonary surfactant protein D suppresses inflammatory cellular responses stimulated with lipopolysaccharide in alveolar macrophages)

    山添 雅己, 西谷 千明, 澤田 格, 光澤 博昭, 清水 健之, 高橋 素子, 高橋 弘毅, 黒木 由夫

    日本生化学会大会・日本分子生物学会年会合同大会講演要旨集   80回・30回   3T22 - 10   2007.11

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  • 肺コレクチンはLegionella pneumophilaに結合する(Pulmonary collectins bind Legionella pneumophila)

    澤田 格, 西谷 千明, 山添 雅己, 光澤 博昭, 清水 健之, 高橋 素子, 村上 聖司, 高橋 弘毅, 黒木 由夫

    日本生化学会大会・日本分子生物学会年会合同大会講演要旨集   80回・30回   4T23 - 7   2007.11

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  • 肺コレクチンとマンノース結合レクチンは異なる機構でToll様受容体に結合する(Lung collectins and mannose binding lectin interact with Toll-like receptors by different mechanisms)

    清水 健之, 西谷 千明, 光澤 博昭, 高橋 素子, 大谷 克城, 若宮 伸隆, 黒木 由夫

    日本生化学会大会・日本分子生物学会年会合同大会講演要旨集   80回・30回   3T22 - 13   2007.11

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  • Toll様受容体4N末端側領域Glu24-Lys47は、MD-2結合部位である(Toll-like receptor 4 region Glu24-Lys47 is a site for MD-2 binding)

    西谷 千明, 高橋 素子, 光澤 博昭, 清水 健之, 佐野 仁美, 松嶋 範男, 黒木 由夫

    日本生化学会大会・日本分子生物学会年会合同大会講演要旨集   80回・30回   3T22 - 12   2007.11

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  • ヒト肺サーファクタントタンパク質Dは糖鎖認識領域を介してMD-2に直接結合する(Human Pulmonary Surfactant Protein D Directly Binds to MD-2 through the Carbohydrate Recognition Domain)

    ニエ・ショウモウ, 西谷 千明, 清水 健之, 光澤 博昭, 山添 雅己, 澤田 格, 高橋 素子, 高橋 弘毅, 黒木 由夫

    日本生化学会大会・日本分子生物学会年会合同大会講演要旨集   80回・30回   3T22 - 11   2007.11

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  • N型糖鎖によるシグナル伝達の制御機構

    高橋 素子, 横江 俊一, 池田 義孝, 谷口 直之, 黒木 由夫

    生化学   79 ( 9 )   903 - 903   2007.9

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  • 【肺の老化を考える】 基礎医学とのダイアローグ 老化とグライケーション

    高橋 素子, 谷口 直之

    THE LUNG-perspectives   15 ( 2 )   203 - 207   2007.4

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  • A secreted type of beta 1,6 N-acetylglucosaminyltransferase V (GnT-V), a novel angiogenesis inducer, is regulated by gamma-secretase (vol 20, pg 2451, 2006)

    Susumu Nakahara, Takashi Saito, Nami Kondo, Kenta Moriwaki, Katsuhisa Noda, Shinji Ihara, Motoko Takahashi, Yoshihito Ide, Jianguo Gu, Hidenori Inohara, Taiichi Katayama, Masaya Tohyama, Takeshi Kubo, Naoyuki Taniguchi, Eiji Miyoshi

    FASEB JOURNAL   21 ( 2 )   630 - 630   2007.2

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  • Development of ELISA for measurement of peroxiredoxin-4 and quantification in rat tissues

    伊東利津, 高橋素子, 高橋素子, 井原秀之, 岡田貴裕, 藤井順逸, 池田義孝

    生化学   2007

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  • ErbB3の二量体形成におけるN型糖鎖の役割

    横江 俊一, 高橋 素子, 朝日 通雄, 顧 建国, 三善 英知, 谷口 直之

    生化学   78 ( 7 )   700 - 700   2006.7

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  • Overexpression of N-acetylglucosaminyltransferase III results in an increasing activity of adenylyl cyclase III

    W Li, M Takahashi, JG Gu, E Miyoshi, Y Shibukawa, N Taniguchi

    GLYCOBIOLOGY   15 ( 11 )   1235 - 1235   2005.11

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  • Core fucosylation of low density lipoprotein receptor-related protein is required for the function as a internalization for IGFBP3

    SH Lee, M Takahashi, E Miyoshi, A Ekuni, T Taguchi, S Inoue, JG Gu, K Honke, N Taniguchi

    GLYCOBIOLOGY   15 ( 11 )   1234 - 1234   2005.11

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  • 【糖鎖と病気】 基礎編 糖鎖シグナル 増殖因子受容体のN型糖鎖の機能

    高橋 素子, 横江 俊一, 谷口 直之

    遺伝子医学MOOK   ( 3 )   164 - 169   2005.9

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  • Overexpression of mutated Cu, Zn-SOD in neuroblastoma cells results in cytoskeletal change (vol 288, pg C253, 2005)

    R Takamiya, M Takahashi, YS Park, Y Tawara, N Fujiwara, Y Miyamoto, J Gu, K Suzuki, N Taniguchi

    AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY   288 ( 6 )   C1461 - C1461   2005.6

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  • 分子生物学 basic technique In vitro翻訳系

    高橋 素子

    THE LUNG-perspectives   12 ( 2 )   207 - 209   2004.4

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  • 増殖因子レセプターのN型糖鎖の機能 (特集 糖鎖の新たな機能と疾患へのかかわり) -- (REVIEW1:糖鎖による制御機構)

    高橋 素子, 本家 孝一, 谷口 直之

    モレキュラ-メディシン   40 ( 9 )   1034 - 1039   2003.9

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  • 【糖鎖の新たな機能と疾患へのかかわり】 増殖因子レセプターのN型糖鎖の機能

    高橋 素子, 本家 孝一, 谷口 直之

    Molecular Medicine   40 ( 9 )   1034 - 1039   2003.8

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  • 可溶型GnT-Vの役割とその分泌機構

    中原 晋, 三善 英知, 斉藤 貴志, 高橋 素子, 野田 勝久, 伊原 伸治, 本家 孝一, 猪原 秀典, 久保 武, 谷口 直之

    日本癌学会総会記事   62回   105 - 105   2003.8

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  • 糖鎖と増殖因子受容体(2)

    高橋 素子

    薬の知識   54 ( 6 )   169 - 169   2003.6

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  • 糖鎖と増殖因子受容体

    高橋 素子

    薬の知識   54 ( 5 )   144 - 144   2003.5

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  • Glycation proceeds faster in mutated Cu, Zn-superoxide dismutases related to familial amyotrophic lateral sclerosis

    R Takamiya, M Takahashi, T Myint, YS Park, N Miyazawa, T Endo, N Fujiwara, H Sakiyama, Y Misonou, Y Miyamoto, J Fujii, N Taniguchi

    FASEB JOURNAL   17 ( 3 )   938 - +   2003.3

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  • Down-regulation of hydrogen peroxide-induced PKC delta activation in N-acetylglucosaminyltransferase III-transfected HeLaS3 cells

    Y Shibukawa, M Takahashi, Laffont, I, K Honke, N Taniguchi

    JOURNAL OF BIOLOGICAL CHEMISTRY   278 ( 5 )   3197 - 3203   2003.1

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  • Downregulation of PKC delta-JNK1 activation and apoptosis induced by hydrogen peroxide in N-acetylglucosaminyltransferase III transfected HeLaS3 cells

    Y Shibukawa, M Takahashi, Laffont, I, K Honke, N Taniguchi

    GLYCOBIOLOGY   12 ( 10 )   693 - 693   2002.10

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  • N型糖鎖修飾酵素の導入によるアデニル酸シクラーゼ活性の修飾

    渋川 幸直, 高橋 素子, 市川 英俊, 本家 孝一, 谷口 直之

    生化学   74 ( 8 )   919 - 919   2002.8

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  • 家族性筋萎縮性側索硬化症における変異Cu,Zn-SOD高発現神経細胞における細胞骨格変化

    高宮 里奈, 高橋 素子, 宮本 泰豪, 藤原 範子, 谷口 直之

    生化学   74 ( 8 )   797 - 797   2002.8

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  • 病理学の挑戦 悪性化ならびに転移の病態の把握に向けて 糖転移酵素によるがん転移の制御とその機構

    谷口 直之, 三善 英知, 北田 学利, 高橋 素子, 池田 義孝, 本家 孝一

    日本癌学会総会記事   60回   34 - 34   2001.9

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  • 家族性筋萎縮性側索硬化症に関連したCu,Zn-SOD変異体のフルクトースによる糖化の亢進

    高宮 里奈, 高橋 素子, 宮澤 伸子, 藤原 範子, 宮本 泰豪, 谷口 直之

    生化学   73 ( 8 )   1070 - 1070   2001.8

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  • 糖転移酵素GnT-III過剰発現HeLaS3細胞におけるEGFレセプターの動態

    佐藤 祐一, 高橋 素子, 渋川 幸直, 石川 睦男, 谷口 直之

    生化学   73 ( 8 )   755 - 755   2001.8

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  • N-アセチルグルコサミン転移酵素III(GnT-III)発現細胞における過酸化水素によるアポトーシスの抑制機構

    渋川 幸直, 高橋 素子, 本家 孝一, 谷口 直之

    生化学   73 ( 8 )   977 - 977   2001.8

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  • 雄ラット生殖器系におけるポリオール代謝酵素の発現と生理的役割

    井内 良仁, 小林 孝至, 金子 智子, 松木 真吾, 高橋 素子, 笹川 五十次, 中田 瑛浩, 藤井 順逸

    生化学   73 ( 8 )   888 - 888   2001.8

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    J-GLOBAL

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  • Overexpression of N-acetylglucosaminyltransferase III enhances the epidermal growth factor-induced phosphorylation of ERK in HeLaS3 cells by up-regulation of the internalization rate of the receptors

    Y Sato, M Takahashi, Y Shibukawa, SK Jain, R Hamaoka, J Miyagawa, Y Yaginuma, K Honke, M Ishikawa, N Taniguchi

    JOURNAL OF BIOLOGICAL CHEMISTRY   276 ( 15 )   11956 - 11962   2001.4

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  • N-アセチルグルコサミン転移酵素(GnT-III)導入HeLaS3細胞におけるEGFシグナリング

    佐藤 祐一, 高橋 素子, 柳沼 裕二, 石川 睦男, 谷口 直之

    日本癌学会総会記事   59回   486 - 487   2000.9

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  • Osmotic stressによるヘパリン結合成EGF様増殖因子(HB-EGF)の発現誘導と作用機序

    高 永鎬, 車 文一, 鈴木 敬一郎, 朴 用軾, 高橋 素子, 東山 繁樹, 谷口 直之

    生化学   72 ( 8 )   907 - 907   2000.8

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  • 家族性筋萎縮性側索硬化症における変異Cu,Zn-SODの糖化反応の亢進

    高宮 里奈, 宮本 泰豪, 高橋 素子, Theingi Myint, 宮澤 伸子, 谷口 直之

    生化学   72 ( 8 )   1064 - 1064   2000.8

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  • 糖転移酵素GnT-III過剰発現細胞におけるEGFシグナリング

    高橋 素子, 佐藤 祐一, 渋川 幸直, 本家 孝一, 谷口 直之

    生化学   72 ( 8 )   983 - 983   2000.8

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  • N-アセチルグルコサミン転移酵素III(GnT III)発現細胞のアポトーシス抑制機構

    渋川 幸直, 高橋 素子, 佐藤 祐一, 本家 孝一, 谷口 直之

    生化学   72 ( 8 )   929 - 929   2000.8

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  • Cloning of amadoriase I isoenzyme from Aspergillus sp.: Evidence of FAD covalently linked to Cys342

    XL Wu, M Takahashi, SG Chen, VM Monnier

    BIOCHEMISTRY   39 ( 6 )   1515 - 1521   2000.2

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  • 医学研究 In vitro kinaseアッセイ

    高橋 素子

    THE LUNG-perspectives   7 ( 4 )   429 - 431   1999.10

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  • 糖転移酵素GnT-III導入CHO細胞におけるEGF受容体の構造変化

    高橋 素子, 渋川 幸直, 井原 祥一, 浜岡 理恵子, 池田 義孝, 谷口 直之

    生化学   71 ( 8 )   853 - 853   1999.8

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  • EGFレセプターに対する糖鎖付加の機能,構造への影響

    津田 岳夫, 池田 義孝, 山口 幸洋, 盛 音, 井原 秀之, 高橋 素子, 谷口 直之

    生化学   71 ( 8 )   1054 - 1054   1999.8

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  • 糖転移酵素GnT-III導入HeLaS3細胞におけるEGF刺激による細胞内情報伝達

    佐藤 祐一, 高橋 素子, Jain Suresh K, 浜岡 理恵子, 池田 義孝, 石川 睦男, 谷口 直之

    生化学   71 ( 8 )   854 - 854   1999.8

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  • Overexpression of the aldose reductase gene induces apoptosis in pancreatic beta-cells by causing a redox imbalance

    R Hamaoka, J Fujii, J Miyagawa, M Takahashi, M Kishimoto, M Moriwaki, K Yamamoto, Y Kajimoto, Y Yamasaki, T Hanafusa, Y Matsuzawa, N Taniguchi

    JOURNAL OF BIOCHEMISTRY   126 ( 1 )   41 - 47   1999.7

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  • A defect in the mitochondrial import of mutant Mn-superoxide dismutase produced in Sf21 cells

    J Fujii, Y Ikeda, T Watanabe, Y Kawasaki, K Suzuki, C Fujii, M Takahashi, N Taniguchi

    JOURNAL OF BIOCHEMISTRY   124 ( 2 )   340 - 346   1998.8

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  • Mn-superoxide dismutase(Mn-SOD)のミトコンドリア移行の変異体を用いた解析

    藤井 順逸, 池田 義隆, 渡辺 俊哉, 川崎 佳巳, 高橋 素子, 鈴木 敬一郎, 谷口 直之

    生化学   70 ( 8 )   988 - 988   1998.8

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  • Selective induction of heparin-binding epidermal growth factor-like growth factor by methylglyoxal and 3-deoxyglucosone in rat aortic smooth muscle cells - The involvement of reactive oxygen species formation and a possible implication for atherogenesis in diabetes

    WY Che, M Asahi, M Takahashi, H Kaneto, A Okado, S Higashiyama, N Taniguchi

    JOURNAL OF BIOLOGICAL CHEMISTRY   272 ( 29 )   18453 - 18459   1997.7

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  • Molecular cloning and expression of amadoriase isoenzyme (fructosyl amine:oxygen oxidoreductase, EC 1.5.3) from Aspergillus fumigatus

    M Takahashi, M Pischetsrieder, VM Monnier

    JOURNAL OF BIOLOGICAL CHEMISTRY   272 ( 19 )   12505 - 12507   1997.5

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  • cDNA cloning of an amadoriase enzyme which cleaves glycated amino acids

    M Takahashi, M Pischetsrieder, VM Monnier

    INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE   38 ( 4 )   5290 - 5290   1997.3

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  • Isolation, purification, and characterization of amadoriase isoenzymes (fructosyl amine-oxygen oxidoreductase EC 1.5.3) from Aspergillus sp

    M Takahashi, M Pischetsrieder, VM Monnier

    JOURNAL OF BIOLOGICAL CHEMISTRY   272 ( 6 )   3437 - 3443   1997.2

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  • ラット大動脈平滑筋細胞におけるメチルグリオキサールによるヘパリン結合性EGF様増殖因子(HB-EGF)の発現誘導とその機序

    車 文一, 朝日 通雄, 高橋 素子, 金藤 秀明, 東山 繁樹, 谷口 直之

    日本分子生物学会年会プログラム・講演要旨集   19   496 - 496   1996.8

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  • Induction of apoptotic cell death by methylglyoxal and 3-deoxyglucosone in macrophage-derived cell lines

    A Okado, Y Kawasaki, Y Hasuike, M Takahashi, T Teshima, J Fujii, N Taniguchi

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   225 ( 1 )   219 - 224   1996.8

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  • 糖尿病ラットにおけるSorbitol dehydrogenaseのグリケーションと不活性化の亢進

    星 歩, 高橋 素子, 藤井 順逸, MYINT Theingi, 谷口 直之

    日本分子生物学会年会プログラム・講演要旨集   19   131 - 131   1996.8

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  • Glycation and inactivation of sorbitol dehydrogenase in normal and diabetic rats

    A Hoshi, M Takahashi, J Fujii, T Myint, H Kaneto, K Suzuki, Y Yamasaki, T Kamada, N Taniguchi

    BIOCHEMICAL JOURNAL   318   119 - 123   1996.8

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  • Deglycating enzymes from Aspergillus sp for potential application in transgenic models of diabetic complications

    M Takahashi, M Pischetsrieder, VM Monnier

    DIABETES   45   812 - 812   1996.5

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    Language：English   Publishing type：Research paper, summary (international conference)  

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  • Induction of aldose reductase gene expression in LEC rats during the development of the hereditary hepatitis and hepatoma

    M Takahashi, A Hoshi, J Fujii, E Miyoshi, T Kasahara, K Suzuki, K Aozasa, N Taniguchi

    JAPANESE JOURNAL OF CANCER RESEARCH   87 ( 4 )   337 - 341   1996.4

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  • FRAGMENTATION OF CERULOPLASMIN FOLLOWING NONENZYMATIC GLYCATION REACTION

    KN ISLAM, M TAKAHASHI, S HIGASHIYAMA, T MYINT, N UOZUMI, Y KAYANOKI, H KANETO, H KOSAKA, N TANIGUCHI

    JOURNAL OF BIOCHEMISTRY   118 ( 5 )   1054 - 1060   1995.11

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  • ELEVATION OF ALDOSE REDUCTASE GENE-EXPRESSION IN RAT PRIMARY HEPATOMA AND HEPATOMA-CELL LINES - IMPLICATION IN DETOXIFICATION OF CYTOTOXIC ALDEHYDES

    M TAKAHASHI, J FUJII, E MIYOSHI, A HOSHI, N TANIGUCHI

    INTERNATIONAL JOURNAL OF CANCER   62 ( 6 )   749 - 754   1995.9

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  • 糖尿病の合併症-glycation 抗ヘキシトールリジン抗体の作製方法とウェスタンブロット法

    高橋 素子, Myint Theingi

    細胞工学   別冊 ( 糖尿病研究ストラテジー )   140 - 142   1995.6

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    Language：Japanese   Publisher：(株)学研メディカル秀潤社  

    Ichushi

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  • 糖尿病の合併症-glycation glycationの中間体代謝酵素

    高橋 素子

    細胞工学   別冊 ( 糖尿病研究ストラテジー )   149 - 150   1995.6

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    Language：Japanese   Publisher：(株)学研メディカル秀潤社  

    Ichushi

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  • IN-VIVO GLYCATION OF ALDEHYDE REDUCTASE, A MAJOR 3-DEOXYGLUCOSONE REDUCING ENZYME - IDENTIFICATION OF GLYCATION SITES

    M TAKAHASHI, YB LU, T MYINT, J FUJII, Y WADA, N TANIGUCHI

    BIOCHEMISTRY   34 ( 4 )   1433 - 1438   1995.1

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  • アルデヒド還元酵素の糖化と不活性化について

    高橋 素子

    生化学   66 ( 12 )   1570 - 1570   1994.12

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    Language：Japanese   Publisher：(公社)日本生化学会  

    Ichushi

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  • 肝細胞癌におけるアルド・ケト還元酵素の動態

    高橋 素子

    日本癌学会総会記事   53回   290 - 290   1994.10

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    Language：Japanese   Publisher：日本癌学会  

    Ichushi

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  • GLYCATION OF HUMAN BETA-(2)-MICROGLOBULIN IN PATIENTS WITH HEMODIALYSIS-ASSOCIATED AMYLOIDOSIS - IDENTIFICATION OF THE GLYCATED SITES

    T MIYATA, R INAGI, Y WADA, Y UEDA, Y IIDA, M TAKAHASHI, N TANIGUCHI, K MAEDA

    BIOCHEMISTRY   33 ( 40 )   12215 - 12221   1994.10

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  • SELECTIVE SUPPRESSION OF IGG2A SUBCLASS IN LEC RATS DURING DEVELOPMENT

    Y IKEDA, T SUGIYAMA, M TAKAHASHI, N TANIGUCHI

    BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS   1200 ( 3 )   277 - 280   1994.8

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  • アルデヒド還元酵素のグライケーションによる不活性化

    高橋 素子

    生化学   65 ( 8 )   902 - 902   1993.8

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    Ichushi

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  • 糖尿病 グリケーションとフリーラジカル 蛋白質変性 特にCu,Zn-SODの断片化と活性酸素生成

    高橋 素子, 谷口 直之

    活性酸素・フリーラジカル   4 ( 2 )   134 - 141   1993.3

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    Ichushi

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  • 糖尿病の集学的管理 フリーラジカルと糖尿病

    谷口 直之, 大河原 知水, 高橋 素子

    綜合臨床   41 ( 9 )   2532 - 2535   1992.9

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    Language：Japanese   Publisher：(株)永井書店  

    Ichushi

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  • 3-デオキシグルコソン還元酵素はアルデヒドレダクターゼと同一である

    高橋 素子

    生化学   64 ( 9 )   1171 - 1171   1992.9

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    Ichushi

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  • 3-デオキシグルコソン還元酵素とアルデヒドレダクターゼの異同についての分子生物学的考察

    高橋 素子

    生化学   64 ( 8 )   713 - 713   1992.8

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Awards

  • Postdoctoral Fellowship Award of Juvenile Diabetes Foundation International›

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Research Projects

  • 高性能イミュノトキシンを用いた小細胞肺がんの標的化治療法の開発

    Grant number：21K08161  2021.4 - 2024.3

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    山口 美樹, 高橋 素子, 佐久間 裕司, 藤谷 直樹, 内田 宏昭

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    Grant amount：\4160000 （ Direct Cost: \3200000 、 Indirect Cost：\960000 ）

    本研究は小細胞肺がんに対する抗体薬物複合体（antibody drug conjugate: ADC）型抗体薬の開発を目的としたモノクローナル抗体の樹立と新規標的の探索である。初年度は、これまでに私たちが樹立したモノクローナル抗体（免疫原：膵臓癌、前立腺癌、肺腺癌、悪性中皮腫、悪性黒色腫、骨髄性白血病、その他の難治性腫瘍、抗原数：68個、抗体数：1200クローン以上）について小細胞肺がん治療における有効性を調査した。小細胞肺がん細胞株であるSBC3、SBC5、NCI-H1092、NCI-H1439、STC1、Lu134AH、MS1L、Lu135、KHM3SおよびNCI-H69について網羅的にフローサイトメトリー（FCM）解析を行った。公共データベースから正常組織および血液系細胞で発現が認められる標的（抗原）について除外した。その結果、調査した全てで強陽性を示したCD#05、CD#55、A#AM10およびJ#M3の4つの抗原が小細胞肺がんに対するADC型抗体薬開発における有望な標的と考えられた。これらの標的に対する内在化能を有するモノクローナル抗体の樹立を現在進めADC型抗体薬の開発に結びつけたい。また、同時に小細胞肺がん細胞株であるSBC5を免疫原とするモノクローナル抗体の樹立も進行中であり、こちらは現時点で内在化能を有する抗体を50個以上樹立出来ており、現在抗原同定を進めているところである。

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  • ErbB4の部位特異的糖鎖解析による糖鎖機能の解明

    Grant number：21K06083  2021.4 - 2024.3

    日本学術振興会  科学研究費助成事業 基盤研究(C)  基盤研究(C)

    高橋 素子, 藤谷 直樹, 上原 康昭, 長谷川 喜弘

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    Grant amount：\4160000 （ Direct Cost: \3200000 、 Indirect Cost：\960000 ）

    ErbBファミリーは、EGFR、ErbB2、ErbB3、ErbB4の４つの分子からなる増殖因子受容体ファミリーである。いずれもがんの発症・進展に深く関与していると考えられている。研究代表者はこれまでにEGFRとErbB3の糖鎖解析を行い、特定の糖鎖構造が機能に関係している可能性を見出した。本研究では、ErbB4の部位特異的糖鎖構造解析を行い、糖鎖によるシグナル制御機構を明らかにすることを目的とする。令和3年度の研究では、以下の結果が得られた。
    １）ErbB4の部位特異的糖鎖付加率および糖鎖構造：CHOK1細胞で発現させたErbB4細胞外ドメインを精製し、LC-ESI-MS/MSを用いて11か所の糖鎖付加部位における糖鎖付加率と糖鎖構造を解析した。N113、N333、N523の３か所はほぼ100%の糖鎖付加率を示した。また、N113、N228、N523の３か所は高マンノース型糖鎖、それ以外の８か所は複合型糖鎖が付加することがわかった。N333上の糖鎖は、他の複合型糖鎖と比較してフコース付加が少ないという特徴がみられた。
    ２）ErbB4の機能に重要な糖鎖の同定：CHOK1細胞を用いてErbBの野生型および糖鎖欠損変異体の安定発現細胞を樹立した。ヘレグリン刺激に対するシグナルを比較する予定である。
    ３）ErbB4細胞外ドメインの糖鎖欠損変異体の性質の評価：ErbB4の細胞外ドメインの野生型および糖鎖欠損変異体の大量調製を行った。ErbB4の細胞外ドメインはEGFシグナルとヘレグリンシグナルの両方を抑制することを確認した。野生型と糖鎖欠損変異体の比較を行う予定である。

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  • Development of a selective culture method for pulmonary epithelial stem cells using high-performance immunotoxin

    Grant number：18K08151  2018.4 - 2021.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    Yamaguchi Miki

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    Grant amount：\4420000 （ Direct Cost: \3400000 、 Indirect Cost：\1020000 ）

    In the respiratory field, idiopathic pulmonary fibrosis or chronic obstructive pulmonary disease is a chronic progressive disease with a poor prognosis for which no cure has been established. We thought that if the lung epithelial stem cells that make up the lung could be transplanted, it could be a new therapeutic method, and devised a selective culture using immunotoxin. By adding CD90-DT3C (immunotoxin), lung epithelial precursors / stem cells could be selectively cultured. In addition, the culture efficiency was further improved by culturing with the addition of A83-01 and Y27632. From the above, selective culture using immunotoxin was completed. We will proceed with the development of a treatment method for chronic obstructive pulmonary disease using this culture system.

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  • Pulmonary fibrosis treatment with pulmonary surfactant as a TLR regulatory molecule and HSP47 inhibition

    Grant number：17K09662  2017.4 - 2020.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    Takahashi Hiroki

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    Grant amount：\4680000 （ Direct Cost: \3600000 、 Indirect Cost：\1080000 ）

    Objective: To develop a new therapeutic method for idiopathic pulmonary fibrosis under the hypothesis that surfactant protein (SP) -A supplementation and HSP47 siRNA suppress lung inflammation and fibrosis. Method: BLM was intratracheally administered to SP-A (-/-) and wild-type mice to prepare a lung injury / fibrosis model, and siRNA HSP47 was intravenously administered. Results: Inflammation and fibrosis were enhanced in SP-A deficient mice compared to wild type. In addition, siRNA HSP47 reduced lung injury and suppressed BLM-induced airway inflammation. Conclusion: SP-A supplementation and siRNA HSP47 suppressed the formation of lung injury / fibrotic lesions, and it was shown that the combination of both could be one of the new treatments for pulmonary fibrosis.

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  • The mechanisms of conformational regulation of ErbB receptors by N-glycans

    Grant number：17K07339  2017.4 - 2020.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)  Grant-in-Aid for Scientific Research (C)

    Takahashi Motoko

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    Grant amount：\4940000 （ Direct Cost: \3800000 、 Indirect Cost：\1140000 ）

    The functional regulation and conformational regulation of growth factor receptors ErbB by N-glycans were examined. N-glycans on EGFR N420, ErbB3 N418, ErbB4 N333 were involved in receptor activation. We examined the site-specific glycosylation status and glycan structures of ErbBs and found that their glycan occupancies were 100% and they were a complex type with little fucose. The signaling inhibitory effects were increased in sEGFR N420Q and sErbB3 N418Q mutants. Although the crystal structure of sErbB3 was not altered by the deletion of N-glycan on N418 by N418Q mutation, the melting temperature of sErbB3 N418Q decreased compared to the wild type, suggesting that this N-glycan contributes to the conformational stability of sErbB3. Taken together, our results suggested that N-glycan on N418 of sErbB3 is involved in the stabilization of structure and that deletion of this glycan increases the structural flexibility which results in facilitation of dimer formation.

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  • Surfactant protein D inhibits activation of non-small cell lung cancer-associated mutant EGFR

    Grant number：16K19461  2016.4 - 2018.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Young Scientists (B)  Grant-in-Aid for Young Scientists (B)

    Hasegawa Yoshihiro, TAKAHASHI MOTOKO, TAKAHASHI HIROKI, SAKUMA YUJI

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    Grant amount：\3900000 （ Direct Cost: \3000000 、 Indirect Cost：\900000 ）

    We have previously demonstrated that SP-D suppressed wild-type EGFR signaling by blocking ligand binding to EGFR. Analysis of patients with lung adenocarcinoma to examine associations between serum SP-D levels and clinical outcome indicated that in TKI-treated patients with lung cancer harboring EGFR mutations, high serum SP-D levels correlated with prolonged overall survival. We herein demonstrate that SP-D downregulates ligand-independent signaling in cells harboring EGFR mutations. SP-D inhibits ligand-independent dimerization of EGFR mutants and dimerization-independent activation of EGFR mutants. SP-D augmented the viability-suppressing effects of EGFR-TKIs. It is possible that the suppressive effects of SP-D on EGF signaling might be implicated in improved clinical outcomes in patients with EGFR mutant lung cancer and high serum SP-D levels.

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  • Suppression of pulmonary injury and fibrosis by applying new action of pulmonary surfactant protein

    Grant number：26461164  2014.4 - 2017.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    TAKAHASHI HIROKI, HASEGAWA YOSHIHIRO, SAITO ATSUSHI

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    Grant amount：\4940000 （ Direct Cost: \3800000 、 Indirect Cost：\1140000 ）

    This study was performed to clarify the importance of pulmonary surfactant protein (SP-A) as an inhibitor of lung injury / fibrosis and allergic airway inflammation and its mechanism, and to show the results that will be a bridge to the therapeutic strategy. In SP-A knockout mice, intrapulmonary inflammation and fibrosis were significantly enhanced under bleomycin stimulation compared with wild type mice. When SP-A was further administered from the respiratory tract, the inflammation was suppressed. Furthermore, in vitro experiments revealed that the inhibitory effect of SP-A against inflammation was based on the inhibition of binding of bleomycin and soluble Toll-like receptor (sTLR2). In addition, the effect of suppressing allergic reaction in respiratory tracts was also confirmed.

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  • The mechanisms of EGF signaling suppression by pulmonary surfactant protein.

    Grant number：26860611  2014.4 - 2016.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Young Scientists (B)  Grant-in-Aid for Young Scientists (B)

    Hasegawa Yoshihiro, MOTOKO TAKAHASHI

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    Grant amount：\3770000 （ Direct Cost: \2900000 、 Indirect Cost：\870000 ）

    Our previous study has indicated that SP-D suppresses EGF signaling by interfering with the ligand-binding to EGFR. SP-D directly binds to the N-glycans of EGFR by lectin activity. In this study, we indicated that SP-A also downregulated EGF signaling by inhibiting ligand-binding to EGFR. In addition, we found that SP-A directly bound to EGFR, but not via N-glycans. Elucidating the antitumor effects of SP-A and SP-D may provide important clues for establishing new therapeutic strategies for lung cancer.

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  • Regulation of ErbB receptors by N-glycans

    Grant number：26440058  2014 - 2016

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)  Grant-in-Aid for Scientific Research (C)

    TAKAHASHI MOTOKO, ARIKI Shigeru, WADA Yoshinao

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    Authorship：Principal investigator  Grant type：Competitive

    Grant amount：\5200000 （ Direct Cost: \4000000 、 Indirect Cost：\1200000 ）

    The fundamental role of the glycan chain is to modify the physicochemical properties of target molecules. The aim of this study is to determine the mechanisms by which N-glycans regulate the function and structure of ErbB. First, we improved the purification efficiency of recombinant soluble ErbB (sErbB) over 100-fold. It was observed that the sEGFR N418Q N-glycan deletion mutant suppressed EGF signaling more effectively than the wild type. The crystal structure of the sErbB3 N418Q N-glycan deletion mutant revealed that the static structure of sErbB3 is not altered by the deletion of the N-glycan. In contrast, the thermostability of sErbB3 N418Q was reduced compared to the wild type. These results indicate that the N-glycan on N418 of ErbB3 is involved in the conformational stability of sErbB3, and the deletion of the N-glycan would increase the flexibility of the molecule.

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  • Studies of pulmonary surfactant proteins on new aspects of host defense functions: anti-tumor activity and defensive activity against disease development.

    Grant number：25461194  2013.4 - 2016.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)  Grant-in-Aid for Scientific Research (C)

    Kuroki Yoshio, TAKAHASHI MOTOKO, ARIKI SHIGERU, HASEGAWA YOSHIHIRO, TAKAMIYA RINA, UEHARA YASUAKI, SAITO ATSUSHI, TAKAHASHI HIROKI

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    Grant amount：\5070000 （ Direct Cost: \3900000 、 Indirect Cost：\1170000 ）

    Pulmonary surfactant proteins, SP-A and SP-D, suppress the growth and progression of lung cancer cells by attenuating the EGF signaling of EGFR phosphorylation and its downstream. SP-D interferes with the EGF binding to EGFR by binding to the high mannose type-sugar moieties of EGFR. SP-A binds to EGFR in a Ca2+-independent manner, indicating the different mechanism from that of SP-D. SP-A and its peptide (SAP01:Tyr161-Lys201) attenuate mast cell migration stimulated with hBD3 and weakened the accumulation of mast cells in the tracheas of asthma model rats. SP-A protein was modified by cigarette smoke extract (CSE) and acrolein containing in the cigarette smoke. The reduction of reactive thiol in the SP-A molecule and the addition of acrolein was observed. The modified SP-A exhibited the decreased ability to attenuate the E. coli growth.

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  • Regulation of ErbB signaling by N-glycan

    Grant number：21590342  2009 - 2011

    Ministry of Education, Culture, Sports, Science and Technology  Grants-in-Aid for Scientific Research(基盤研究(C))  基盤研究(C)

    Motoko TAKAHASHI, Chiaki NISHITANI

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    Authorship：Principal investigator  Grant type：Competitive

    Grant amount：\4420000 （ Direct Cost: \3400000 、 Indirect Cost：\1020000 ）

    The aim of this study is to understand the mechanisms by which N-glycan regulate function and structure of ErbB. We prepared the extracellular domain of ErbB(sErbB) and N418Q mutant of ErbB3. sErbB3 suppressed heregulin signaling more effectively than ErbB2 or ErbB4, and N418Q mutant suppressed more than wild type. Cell proliferation-inhibitory activity of sErbB3 was also upregulated by N418Q mutation. The results indicate that N-glycan on Asn418 of ErbB3 regulates the ErbB3 signaling.

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  • Mechanisms of host defense against pulmonaryinfection, inflammation and injury by surfactant proteins and studies on clinical applications

    Grant number：20390232  2008 - 2010

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (B)

    KUROKI Yoshio, TAKAHASHI Motoko, SHIMIZU Takeyuki, NISHITANI Chiaki, ARIKI Shigeru

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    Grant amount：\18590000 （ Direct Cost: \14300000 、 Indirect Cost：\4290000 ）

    Pulmonary surfactant is composed of lipids and proteins, and plays important roles in alveolar stability and in host defense of respiratory system. In this study, we made specific antibody against human SP-C, which can be used for clinical applications. In addition, SP-A and SP-D, pulmonary collectins, have been shown to directly bind to Legionella pneumophila and Mycobacterium avium, suppress their growth and inhibit cellular injuries caused by these bacteria. SP-D has been found to inhibit matrix metallo-proteinase activity in alveolar macrophages, These results established the molecular bases for clinical applications of the uses of surfactant proteins.

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  • 肺コレクチンを介するマクロファージ細菌貪食の分子機構

    Grant number：19041062  2007 - 2008

    日本学術振興会  科学研究費助成事業  特定領域研究

    黒木 由夫, 高橋 素子, 清水 健之, 光澤 博昭, 西谷 千明

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    Grant amount：\8500000 （ Direct Cost: \8500000 ）

    肺コレクチンのSP-AとSP-Dは、生体防御レクチンとして呼吸器の自然免疫生体防御を担っている。本研究の目的は、肺コレクチンを介するマクロファージ細菌貪食とコレクチン・細菌相互作用の分子機構を解明し、感染現象における肺コレクチンの機能を明らかにすることである。以下に今年度の研究成果を要約する。
    1. 肺コレクチンは、レジオネラ菌の増殖をカルシウム依存性に抑制した。また、レジオネラ菌由来リボ多糖(LPS)は、肺コレクチンのリガンドであり、LPSの添加によって肺コレクチンによるレジオネラ菌増殖抑制効果が失われたので、肺コレクチンによるレジオネラ菌増殖抑制作用には、コレクチンとLPSとの相互作用が重要であることが示唆された。
    2. IV型分泌機構によるレジオネラ菌のマクロファージ傷害活性(pore-forming activity)について、肺コレクチン存在下でレジオネラ菌をマクロファージに感染させると、傷害細胞膜を有するマクロファージ数が有意に低下していた。このことは肺コレクチンがレジオネラ菌によるproe-forming activityを抑制することを示している。
    3. レジオネラ菌を30分間感染させたマクロファージを0〜4日間培養したところ、感染直後のマクロファージでは肺コレクチン存在下での感染で有意に多くの菌がマクロファージに取り込まれていたが、感染2-4日で、マクロファージ内で生存している菌数は有意に低下していた。このことは、肺コレクチンがレジネラ菌の細胞内増殖を抑制することを示している。
    4. 酸性で蛍光を発するpHrodo標識レジオネラ菌を肺コレクチン存在下でマクロファージに感染させたところ、蛍光陽性マクロファージ数が有意に増加していた。このことは、肺コレクチン存在下ではレジオネラ菌含有ファゴソームがリソソームと融合し、レジオネラ菌の酸化が促進されたことを示唆している。

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  • Host defense system in the lung using pulmonary surfactant proteins and Toll-like reosptors

    Grant number：18390241  2006 - 2007

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)  Grant-in-Aid for Scientific Research (B)

    KUROKI Yoshio, TAKAHASHI Hiroki, TAECAHASHI Motoko, SHIMIZU Takeyuki, MITSUZAWA Hiroaki, NISHITANI Chiaki

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    Grant amount：\17380000 （ Direct Cost: \15400000 、 Indirect Cost：\1980000 ）

    The purposes of this project were to investigate the mechanisms by which pulmonary collections, surfactant proteins A and D (SP-A and SP-D), and Toll-like receptor (TISO function against infection and inflammation, and to establish the molecular basis for the clinical application of these proteins. The research results are summarized below.
    1. We have found that SP-A and SP-D bind to TLR2, TLR4 and MD-2. SP-A inhibited the binding of smooth LPS on the cells expressing TLR4 and MD-2 and suppresses inflammation elicited by smooth LPS. The functional domain was the carbohydrate recognition domain (CRD) of SP-A, but the collagenase-resistant fragment of SP-A (CRF) in which the collagenous domain was removed bound to TLR4 very weakly and did not inhibit LPS-induced inflammation, indicating that the oligometric structure composed of SP-A octadecamers is important for expressing its function. Unlike SP-A SP-D inhibits inflammation elicited by different serotypes of LPS, rough LPS and smooth LPS. The experiments with SP-A/SP-D chimeric proteins revealed that the cruciform structure of SP-D composed of long collagenous domain was crucial for suppressing inflammation.
    2. We have also found that the amino-terminal region of TLR4, Glu24-Lys47, is a site for MD-2 binding. Recombinant soluble forms of the extracellular TLR4 domain and MD-2 were demonstrated to dampen endotoxin-induced pulmonary inflammation in mice.
    3. The experiments with TLR4 mutant, TLR4C88A, revealed that MD-2 possesses crucial abilities to express cell surface expression of TLR4 and its N-linked complex type glyoosylation.
    4. SP-A and SP-D bound to Mycobacterium avium and induced bacrerial aggregation. SP-D possesses a potent ability to aggregate M. avium compared with SP-A The ligand for SP-D on M. avium was lipoarabinomannan (LAM) and that for SP-Aexisted in the lipid fraction extracted M. avium.

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  • Functional Regulation of Erb B family by N-glycosylation

    Grant number：18590272  2006 - 2007

    Ministry of Education, Culture, Sports, Science and Technology  Grants-in-Aid for Scientific Research(基盤研究(C))  基盤研究(C)

    Motoko TAKAHASHI

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    Authorship：Principal investigator  Grant type：Competitive

    Grant amount：\3300000 （ Direct Cost: \3000000 、 Indirect Cost：\300000 ）

    Glycosylation is one of the most common post-translational modification, and is known to change physico-chemical properties of proteins. In this study, I examine the function of N-glycan of ErbB family and adenylyl cyclase.ErbB3 has 10 potential glycosylation sites in its extracellular domain. A series of human ErbB3 molecules devoid of N-glycan were prepared and transfected to Flp-In-CHO cells for stable expression. It was revealed that the Asn 418 to Gln mutant (N418Q) mutant of ErbB3 underwent ligand-independent homodimerization. When overexpressed with ErbB2, ligand-independent hetero-dimerization was observed and Erk and Akt phosphorylation was upregulated in the absence of of ErbB3 coexpressed with ErbB2 promoted cell proliferation and colony formation in soft agar in an Erk and Akt-dependent manner. The N418Q mutation also promoted the growth of tumors in athymic mice when injected subcutaneously. Thus, Asn 418-linked N-glycan in ErbB3 plays an essential role in regulating receptor heterodimerization with ErbB2 and might have an effect on transforming activity.Adenylyl cyclase III (ACIII) has 2 potential glycosylation sites in its extracellular domain, and it was suggested that glycosylation is involved in its enzymatic activity. When processing of glycosylation was suppressed by introducing GnT-III, one of glycosyltransferases, forskolin-induced ACIII activation and downstream signaling such as the synthesis of cAMP and the phosphorylation of CREB were significantly upregulated. Now the mechanisms of the regulation of ACIII by the structure of N-glycan is being investigated.

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  • ErbBファミリーの二量体形成におけるN型糖鎖の機能

    Grant number：16790167  2004 - 2005

    文部科学省  科学研究費補助金(若手研究(B))  若手研究(B)

    高橋 素子

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    Authorship：Principal investigator  Grant type：Competitive

    Grant amount：\3100000 （ Direct Cost: \3100000 ）

    N型糖鎖は、タンパクの構造や可塑性、親水性を変化させ、その機能を修飾することが明らかとなっているが、シグナル分子における役割はいまだ明確ではない。本研究ではモデルの糖タンパクとしてErbBファミリーを選び、その二量体形成におけるN型糖鎖の役割を検討した。EGFRでは、そのドメインIIIの糖鎖のうち、Asn420に付加する糖鎖を失うとリガンド非依存性に二量体を形成することがわかっている。ドメインIIIの構造がEGFRと比較的似ているErbB3で、EGFRのAsn420に相当するAsn418をGlnに変えN型糖鎖の付加部位を欠失させると、やはりリガンド非依存性に二量体を形成することがわかった。このN418Q変異ErbB3をErbB2と共発現させた細胞では、Erkのリン酸化が著明に上昇し、ErbB3ホモ二量体のみならずErbB2-ErbB3のヘテロ二量体形成も増加することがわかった。さらに、この下流のシグナルの増強により足場非依存性の増殖能を獲得すること、ヌードマウスにおける腫瘍形成能が著しく上昇することが明らかとなった。一方、ErbB2においてはドメインIIIにN型糖鎖の付加部位は存在しないが、EGFRのAsn420、ErbB3のAsn418に相当する部位に糖鎖の付加部位を導入したG449N変異ErbB2では、リガンド非依存性の二量体形成が減少することがわかった。ErbB2の立体構造は、EGFRやErbB3にリガンドが結合したときの構造に近いことが報告されている。今後、EGFRやErbB3ではドメインIIIの糖鎖を除くとリガンドが結合したときと近い立体構造をとること、またErbB2ではドメインIIIの糖鎖がないことがリガンド非依存性の二量体形成や細胞の増殖能といった癌原性を示す原因になっていることを証明したい。

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  • Integrated analyses of biological functions of sugar chains : Glycomics

    Grant number：13854010  2001 - 2005

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (S)  Grant-in-Aid for Scientific Research (S)

    TANIGUCHI Naoyuki, MIYOSHI Eiji, HONKE Koichi, JIANGUO Gu, BUNGYOKU Tei, TAKAHASHI Motoko

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    Grant amount：\122980000 （ Direct Cost: \94600000 、 Indirect Cost：\28380000 ）

    To know biological functions of sugar chain by integrated analyses, we have identified target glycoproteins of specific glycosyltransferases as follows.
    GnT-V catalyses the synthesis of beta 1-6 GlcNAc branching which involves inn tumor metastasis and invasion. In this project, we identified matriptase as a target molecule of GnT-V, which can activate uPA, and HGF. Addition of betal-6 GlcNAc branching on matriptase brought prolonged degradation of these proteins, leading to tumor metastasis in nude mice experiments.
    Cadherin and integrin are target molecules for GnT-III which involves in the synthesis of bisecting GlcNAc structure. Bisecting GlcNAc inhibit further processing of N-glycan elongation via GnT-V or GnT-IV. In this project, biological functions of sugar chains on integrin and ECM interaction were clarified as a level of purified molecules. Cadherin/beta catenin system is also regulated by GnT-III. Phosphorylation of beta-catenin is suppressed by GnT-III and expression of e-cadherin is controlled by GnT-III
    Fut8 involves in core fucosylation on N-glycans. To know physiological meaning of Fut8, we established Fut8 deficient mice. This mouse shows severe growth retardation and 70% of mice die within 3 days after birth. Interestingly, pathological analysis showed emphysema-like lesion in lung of the mice. The mechanism underlying this change is due to dys-regulation of TGF beta-receptor, leading to increases in MMP expression.

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  • 糖鎖構造リモデリングによるEGFレセプターのエンドサイトーシスの制御

    Grant number：13770058  2001 - 2002

    文部科学省  科学研究費補助金(奨励研究(A), 若手研究(B))  奨励研究(A), 若手研究(B)

    高橋 素子

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    Authorship：Principal investigator  Grant type：Competitive

    Grant amount：\2100000 （ Direct Cost: \2100000 ）

    本研究ではCHO-HER細胞にGnT-III遺伝子を導入することによって、EGFシグナル経路や受容体のエンドサイトーシスにどのような変化が起こるかを検討した。^<125>I-EGFを用いたリガンド結合実験によって、GnT-III導入細胞ではEGF受容体のうち低親和性のものが減少することがわかった。またGnT-III導入細胞では受容体のエンドサイトーシスが亢進することが明らかとなった。そこで糖鎖の改変したEGF受容体を精製し解析するため、EGF受容体にHis-tagをつけたものをCHO細胞に導入し、CHO-HER(His)細胞を確立した後GnT-III遺伝子を導入した。この細胞抽出液より金属キレートカラムと抗体カラムを用いることによってEGF受容体を精製した。現在、この精製物と人工脂質重膜を用いて細胞膜を再構成することを試みている。また一方で、EGFRをGFPにて蛍光ラベルし、GnT-IIIを同時にCHO細胞に導入したものを用いて一分子解析を試みている。

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  • 新しいトランスメンブランシグナリングとしての糖鎖シグナルネットワーク

    Grant number：13307007  2001

    日本学術振興会  科学研究費助成事業 基盤研究(A)  基盤研究(A)

    谷口 直之, 鄭 文玉, 三善 英知, 本家 孝一, 宮本 泰豪, 高橋 素子

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    Grant amount：\34320000 （ Direct Cost: \26400000 、 Indirect Cost：\7920000 ）

    本研究は、糖鎖遺伝子のマニピュレーションによる糖鎖構造改変が細胞応答や細胞機能の制御に及ぼす影響を分子レベルで解明することを目的として、具体的には、EGF受容体、カドヘリン-カテニン系、血管新生因子、マトリックス分解プロテアーゼの機能制御に関して解析を開始した。成果の一部は、5月にスイスで開催された「Protein traffic, Glycosylation, and Human Health」に関する国際シンポジウムで発表され、諸外国の一線の研究者と糖鎖の機能に関して、最新の情報が交わされた。この後急遽、基盤研究(S)「糖鎖機能の統合的把一握:グライコミクス」(課題番号13854010)(平成13年度〜平成17年度)が採択されたので、本研究はそちらで発展継続することとなった。

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  • 受容体チロシンキナーゼEGFレセプターの糖鎖構造のリモデリングによる増殖制御

    Grant number：11770062  1999 - 2000

    文部科学省  科学研究費補助金(奨励研究(A))  奨励研究(A)

    高橋 素子

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    Authorship：Principal investigator  Grant type：Competitive

    Grant amount：\2100000 （ Direct Cost: \2100000 ）

    本研究ではHeLaS3細胞にGnT-III遺伝子を導入することによって、EGFシグナル経路にどのような変化が起こるかを検討した。^<125>I-EGFを用いた実験によってGnT-III導入細胞ではEGFレセプターのEGF結合能が低下していることが明らかとなったが、スキャッチャード解析により、これは主に低親和性受容体の減少によるものであることがわかった。高親和性受容体には変化がみられず、EGFレセプターの自己リン酸化の程度には変化がないことがわかった。一方、GnT-III導入細胞では受容体のエンドサイトーシスが亢進し、ERKの活性化が上昇することが明らかとなった。受容体のエンドサイトーシスの変化の機序を検討したところ、GnT-III導入細胞ではエンドサイトーシスに関与すると考えられているEGFレセプターのCaInドメイン中の^<996>Q-^<1022>Tに修飾がおこっていることが示唆された。この^<996>Q-^<1022>Tという配列はEGFレセプターの細胞内ドメインに存在するため、糖鎖に直接関係した修飾ではないと考えられる。現在精製EGFレセプターのペプチドマッピングをおこなうことにより、その修飾の位置と種類の同定を行っている。今後、この修飾がEGFシグナル経路にどのように影響するかをさらに検討する予定である。

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  • Redox regulation by glutathione and the roles of reactive oxygen and nitrogen species

    Grant number：10044286  1998 - 2000

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (A)

    TANIGUCHI Naoyuki, FUJII Junichi, SUZUKI Keiichiro, HIGASHIYAMA Shigeki, IKEDA Yoshitaka, TAKAHASHI Motoko

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    Grant amount：\15500000 （ Direct Cost: \15500000 ）

    Reactive oxygen species(ROS) such as the superoxide anion (O_2^-), hydrogen peroxide (H_2O_2) and the hydroxyl radical (OH) are represent putative biohazards when present in excess, a condition which,is referred to as "oxidative stress". ROS are generated within cells as byproducts of biological oxidations and are thought to play important roles in several pathophysiologic events, including inflammation, mutagenesis, and aging. Recently ROS and redox balance are thought to act as an intracellular signal and have a wide variety of biological action. So in this project we have demonstrated new biological functions of ROS, glutathione and redox balance.
    1)Inactivation of glutathine peroxidase by reducing sugars and dicarbonyl compounds
    2)New biological faction of peroxiredixin family : Purification and cloning of peroxiredoxin IV and its antioxidative property in extracellular space
    3)Ceruloplasmin(Cp) has a glutathione peroxidase-like activity together with its ferroxidase activity and would completely remove the primary reactants required for both Fenton chemistry and lipid peroxidation. And Cp binds to extracellular myeloperoxidase(MPO) and prevents MPO making HOC1, a powerful oxidant which will lead to molecular damage.
    4)Hydroxyl radicals accelerates the adhesion of neutrophils and cancer cells to endothelial cells in the absence of de novo protein synthesis
    5)Mechanisms of anti-oxidative functions of glutathione, giutathione peroxidase and γ GCS, especially involvement of signal transduction.
    6)Nitric oxide inactivates glutathione peroxidase and the accumulated hydrogen peroxide induces Heparin-binding EGF-like growth factor(HB-EGF) as an autocrine protective factor in rat aortic smooth muscle cells via the JNK pathway.

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  • Glycobiology in signalling

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    Grant type：Competitive

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  • Diabetes and Glycation

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    Grant type：Competitive

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  • 糖鎖構造のシグナル伝達に与える影響

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    Grant type：Competitive

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  • 糖尿病とグリケーション

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    Grant type：Competitive

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