Updated on 2026/02/10

写真a

 
ARIKI Shigeru
 
Organization
Medical Development Center Dean Department of Liberal Arts and Sciences Chemistry Associate Professor
Title
Associate Professor
Homepage
https://smu-chemistry.wixsite.com/sapmed-chemistry
External link

Degree

  • Master(Science) ( Kyushu University )

  • 博士（理学） ( 九州大学 )

Research Interests

  • innate immunity

  • 自然免疫

Research Areas

  • Life Science / Medical biochemistry

  • Life Science / Functional biochemistry

Education

  • 九州大学大学院   理学府   生物科学

    - 2006

    　 More details

    Country： Japan

    researchmap

  • 九州大学大学院   理学府   生物科学

    - 2003

    　 More details

    Country： Japan

    researchmap

  • Kyushu University   School of Sciences

    - 2001

    　 More details

    Country： Japan

    researchmap

Research History

  • 札幌医科大学医療人育成センター   教養教育研究部門   准教授

    2015.4

    　 More details

  • 札幌医科大学医学部   医化学講座   講師

    2012.8 - 2015.3

    　 More details

  • 札幌医科大学医学部   医化学講座   助教

    2007.8 - 2012.7

    　 More details

  • 九州大学大学院理学研究院   学術研究員

    2007.4 - 2007.7

    　 More details

  • 日本学術振興会特別研究員

    2005.4 - 2007.3

    　 More details

Professional Memberships

Papers

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

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

    Glycobiology   34 ( 3 )   2024.4

    　More details

    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

    PubMed

    researchmap

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

    　More details

    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

    PubMed

    researchmap

  • N-glycosylation regulates MET processing and signaling. Reviewed 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

    　More details

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

    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

    PubMed

    researchmap

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

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

    Biochemistry   60 ( 21 )   1708 - 1721   2021.6

    　More details

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

    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

    PubMed

    researchmap

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

    　More details

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

    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.

    DOI： 10.1016/j.bbagen.2020.129699

    PubMed

    researchmap

  • 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

    　More details

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

    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

    PubMed

    researchmap

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

    Youhei Takahashi, Atsushi Saito, Hirofumi Chiba, Koji Kuronuma, Kimiyuki Ikeda, Tomofumi Kobayashi, Shigeru Ariki, Motoko Takahashi, Yasushi Sasaki, Hiroki Takahashi

    Respiratory research   19 ( 1 )   34 - 34   2018.2

    　More details

    Language：English  

    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.

    DOI： 10.1186/s12931-018-0736-9

    PubMed

    researchmap

  • 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

    　More details

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

    DOI： 10.1074/jbc.M117.800771

    PubMed

    Web of Science

    researchmap

  • 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

    　More details

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

    DOI： 10.1038/onc.2017.253

    PubMed

    Web of Science

    researchmap

  • 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

    　More details

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

    DOI： 10.1038/s41598-017-08588-5

    PubMed

    Web of Science

    researchmap

  • 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

    　More details

    Authorship：Last author,　Corresponding author   Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.4049/jimmunol.1502626

    PubMed

    Web of Science

    researchmap

  • 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

    　More details

    Authorship：Last author,　Corresponding author   Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1016/j.bbrc.2017.02.028

    PubMed

    Web of Science

    researchmap

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

    Ito E, Oka R, Ishii T, Korekane H, Kurimoto A, Kizuka Y, Kitazume S, Ariki S, Takahashi M, Kuroki Y, Kida K, Taniguchi N

    Data in brief   5   707 - 711   2015.12

    　More details

  • 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

    　More details

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

    DOI： 10.1016/j.jprot.2015.07.011

    PubMed

    Web of Science

    researchmap

  • 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

    　More details

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

    DOI： 10.1038/onc.2014.20

    PubMed

    Web of Science

    researchmap

  • Distinct compartmentalization of SP-A and SP-D in the vasculature and lungs of patients with idiopathic pulmonary fibrosis Reviewed

    Hirotaka Nishikiori, Hirofumi Chiba, Shigeru Ariki, Koji Kuronuma, Mitsuo Otsuka, Masanori Shiratori, Kimiyuki Ikeda, Atsushi Watanabe, Yoshio Kuroki, Hiroki Takahashi

    BMC PULMONARY MEDICINE   14   196   2014.12

    　More details

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

    DOI： 10.1186/1471-2466-14-196

    PubMed

    Web of Science

    researchmap

  • 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

    　More details

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

    DOI： 10.1016/j.bbrc.2014.10.086

    PubMed

    Web of Science

    researchmap

  • 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

    　More details

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

    DOI： 10.1074/jbc.M113.491902

    PubMed

    researchmap

  • 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

    　More details

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

    DOI： 10.1074/jbc.M112.380287

    PubMed

    Web of Science

    researchmap

  • In vivo role of aldehyde reductase Reviewed

    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

    　More details

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

    DOI： 10.1016/j.bbagen.2012.07.003

    Web of Science

    researchmap

  • Implication of Antigenic Conversion of Helicobacter pylori Lipopolysaccharides That Involve Interaction with Surfactant Protein D Reviewed

    Shin-ichi Yokota, Ken-ichi Amano, Chiaki Nishitani, Shigeru Ariki, Yoshio Kuroki, Nobuhiro Fujii

    INFECTION AND IMMUNITY   80 ( 8 )   2956 - 2962   2012.8

    　More details

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

    DOI： 10.1128/IAI.00345-12

    PubMed

    Web of Science

    researchmap

  • 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

    　More details

    Authorship：Lead author,　Corresponding author   Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1074/jbc.M111.308056

    PubMed

    Web of Science

    researchmap

  • Diverse Functions of Pulmonary Collectins in Host Defense of the Lung Reviewed

    Shigeru Ariki, Chiaki Nishitani, Yoshio Kuroki

    JOURNAL OF BIOMEDICINE AND BIOTECHNOLOGY   2012   532071   2012

    　More details

    Authorship：Lead author,　Corresponding author   Language：English  

    DOI： 10.1155/2012/532071

    PubMed

    Web of Science

    researchmap

  • 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

    　More details

    Authorship：Lead author,　Corresponding author   Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.4049/jimmunol.1100024

    PubMed

    Web of Science

    researchmap

  • Protein Crosslinking by Transglutaminase Controls Cuticle Morphogenesis in Drosophila Reviewed

    Toshio Shibata, Shigeru Ariki, Naoaki Shinzawa, Ryuta Miyaji, Haruka Suyama, Miyuki Sako, Nobuyuki Inomata, Takumi Koshiba, Hirotaka Kanuka, Shun-ichiro Kawabata

    PLOS ONE   5 ( 10 )   e13477   2010.10

    　More details

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

    DOI： 10.1371/journal.pone.0013477

    PubMed

    Web of Science

    researchmap

  • 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

    　More details

    Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1074/jbc.M109.074765

    PubMed

    Web of Science

    researchmap

  • 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

    　More details

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

    DOI： 10.1016/j.bbagen.2009.10.006

    Web of Science

    researchmap

  • 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

    　More details

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

    DOI： 10.1093/intimm/dxp059

    PubMed

    Web of Science

    researchmap

  • Factor C Acts as a Lipopolysaccharide-Responsive C3 Convertase in Horseshoe Crab Complement Activation Reviewed

    Shigeru Ariki, Shusaku Takahara, Toshio Shibata, Takaaki Fukuoka, Aya Ozaki, Yuichi Endo, Teizo Fujita, Takumi Koshiba, Shun-ichiro Kawabata

    JOURNAL OF IMMUNOLOGY   181 ( 11 )   7994 - 8001   2008.12

    　More details

    Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.4049/jimmunol.181.11.7994

    PubMed

    Web of Science

    researchmap

  • 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

    　More details

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

    DOI： 10.1074/jbc.M807268200

    PubMed

    Web of Science

    researchmap

  • 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

    　More details

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

    DOI： 10.1021/bi8010175

    PubMed

    Web of Science

    researchmap

  • Recognition of pathogens and activation of immune responses in Drosophila and horseshoe crab innate immunity Reviewed

    Shoichiro Kurata, Shigeru Ariki, Shun-ichiro Kawabata

    IMMUNOBIOLOGY   211 ( 4 )   237 - 249   2006

    　More details

  • An antimicrobial peptide tachyplesin acts as a secondary secretagogue and amplifies lipopolysaccharide-induced hemocyte exocytosis. Reviewed International journal

    Aya Ozaki, Shigeru Ariki, Shun-Ichiro Kawabata

    The FEBS journal   272 ( 15 )   3863 - 71   2005.8

    　More details

    Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)  

    In the horseshoe crab, bacterial lipopolysaccharide (LPS) induces exocytosis by granular hemocytes, resulting in the secretion of various defense molecules, such as lectins and antimicrobial peptides, via a G protein-mediating signaling pathway. This response is a key component of the horseshoe crab innate immune response against infectious microorganisms. Here, we report an endogenous amplification mechanism for LPS-induced hemocytes exocytosis. The concentration of LPS required for maximal secretion decreased in proportion to the density of hemocytes, suggesting the presence of a positive feedback mechanism for secretion via a mediator secreted from hemocytes. The exocytosed fluid of hemocytes was found able to induce hemocyte exocytosis in the absence of LPS. Furthermore, tachyplesin, a major antimicrobial peptide of hemocytes, was able to trigger exocytosis in an LPS-independent manner, which was inhibited by a phospholipase C inhibitor, U-73122, and a G protein inhibitor, pertussis toxin. Surface plasmon resonance analysis showed that tachyplesin directly interacts with bovine G protein. These findings suggest that the tachyplesin-induced hemocyte exocytosis also occurs via a G protein-mediating signaling pathway. We concluded that tachyplesin functions not only as an antimicrobial substance, but also as a secondary secretagogue of LPS-induced hemocyte exocytosis, leading to the amplification of the innate immune reaction at sites of injury.

    PubMed

    researchmap

  • A Toll-like receptor in horseshoe crabs. Reviewed International journal

    Kei-ichiro Inamori, Shigeru Ariki, Shun-ichiro Kawabata

    Immunological reviews   198   106 - 15   2004.4

    　More details

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

    Non-self-recognition of invading microbes relies on the pattern-recognition of pathogen-associated molecular patterns (PAMPs) derived from microbial cell-wall components. Insects and mammals conserve a signaling pathway of the innate immune system through cell-surface receptors called Tolls and Toll-like receptors (TLRs). Bacterial lipopolysaccharides (LPSs) are an important trigger of the horseshoe crab's innate immunity to infectious microorganisms. Horseshoe crabs' granular hemocytes respond specifically to LPS stimulation, inducing the secretion of various defense molecules from the granular hemocytes. Here, we show a cDNA which we named tToll, coding for a TLR identified from hemocytes of the horseshoe crab Tachypleus tridentatus. tToll is most closely related to Drosophila Toll in both domain architecture and overall length. Human TLRs have been suggested to contain numerous PAMP-binding insertions located in the leucine-rich repeats (LRRs) of their ectodomains. However, the LRRs of tToll contained no obvious PAMP-binding insertions. Furthermore, tToll was non-specifically expressed in horseshoe crab tissues. These observations suggest that tToll does not function as an LPS receptor on granular hemocytes.

    PubMed

    researchmap

  • A serine protease zymogen functions as a pattern-recognition receptor for lipopolysaccharides. Reviewed International journal

    Shigeru Ariki, Kumiko Koori, Tsukasa Osaki, Kiyohito Motoyama, Kei-ichiro Inamori, Shun-ichiro Kawabata

    Proceedings of the National Academy of Sciences of the United States of America   101 ( 4 )   953 - 8   2004.1

    　More details

    Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)  

    Bacterial lipopolysaccharide (LPS)-induced exocytosis of granular hemocytes is a key component of the horseshoe crab's innate immunity to infectious microorganisms; stimulation by LPS induces the secretion of various defense molecules from the granular hemocytes. Using a previously uncharacterized assay for exocytosis, we clearly show that hemocytes respond only to LPS and not to other pathogen-associated molecular patterns, such as beta-1,3-glucans and peptidoglycans. Furthermore, we show that a granular protein called factor C, an LPS-recognizing serine protease zymogen that initiates the hemolymph coagulation cascade, also exists on the hemocyte surface as a biosensor for LPS. Our data demonstrate that the proteolytic activity of factor C is both necessary and sufficient to trigger exocytosis through a heterotrimeric GTP-binding protein-mediating signaling pathway. Exocytosis of hemocytes was not induced by thrombin, but it was induced by hexapeptides corresponding to the tethered ligands of protease-activated G protein-coupled receptors (PARs). This finding suggested the presence of a PAR-like receptor on the hemocyte surface. We conclude that the serine protease zymogen on the hemocyte surface functions as a pattern-recognition protein for LPS.

    PubMed

    researchmap

▼display all

MISC

  • 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

    　More details

    Language：Japanese   Publisher：生命科学系学会合同年次大会運営事務局  

    Ichushi

    researchmap

  • 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

    　More details

    Language：Japanese  

    J-GLOBAL

    researchmap

  • 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

    　More details

    Language：Japanese   Publisher：(株)先端医学社  

    Ichushi

    researchmap

  • 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

    　More details

    Language：Japanese   Publisher：(株)先端医学社  

    Ichushi

    researchmap

  • 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

    　More details

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

    Ichushi

    J-GLOBAL

    researchmap

  • 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

    　More details

    Language：Japanese  

    J-GLOBAL

    researchmap

  • 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

    　More details

    Language：Japanese   Publisher：(株)先端医学社  

    Ichushi

    researchmap

  • 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

    　More details

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

    Ichushi

    J-GLOBAL

    researchmap

  • 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

    　More details

    Language：Japanese   Publisher：医学図書出版(株)  

    Ichushi

    researchmap

  • 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

    　More details

    Language：Japanese   Publisher：(一社)日本泌尿器科学会総会事務局  

    Ichushi

    researchmap

  • 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

    　More details

    Language：Japanese   Publisher：(一社)日本呼吸器学会  

    Ichushi

    researchmap

  • 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

    　More details

    Language：Japanese   Publisher：(公社)日本化学療法学会  

    Ichushi

    researchmap

  • 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

    　More details

    Language：Japanese   Publisher：(株)先端医学社  

    Ichushi

    researchmap

  • 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

    　More details

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

    Web of Science

    researchmap

  • 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

    　More details

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

    Web of Science

    researchmap

  • 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

    　More details

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

    Ichushi

    researchmap

  • 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

    　More details

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

    Ichushi

    researchmap

  • 【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

    　More details

    Language：Japanese   Publisher：(有)科学評論社  

    Ichushi

    researchmap

  • 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

    　More details

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

    Web of Science

    researchmap

  • 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

    　More details

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

    Web of Science

    researchmap

  • 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

    　More details

    Language：Japanese   Publisher：医学図書出版(株)  

    Ichushi

    researchmap

  • 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

    　More details

    Language：Japanese   Publisher：緑膿菌感染症研究会  

    Ichushi

    researchmap

  • 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

    　More details

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

    Ichushi

    researchmap

  • 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

    　More details

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

    Ichushi

    researchmap

  • 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

    　More details

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

    Ichushi

    researchmap

  • 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

    　More details

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

    Ichushi

    researchmap

  • 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

    　More details

    Language：Japanese   Publisher：ライフサイエンス出版(株)  

    Ichushi

    researchmap

  • 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

    　More details

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

    Ichushi

    researchmap

  • 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

    　More details

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

    Ichushi

    researchmap

  • 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

    　More details

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

    Ichushi

    researchmap

  • 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

    　More details

    Language：Japanese   Publisher：(一社)日本臨床化学会  

    Ichushi

    researchmap

  • 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

    　More details

    Language：Japanese   Publisher：(株)先端医学社  

    Ichushi

    researchmap

  • ピロリ菌リポ多糖の抗原性変化―サーファクタント蛋白質との相互作用と病原性との関連性―

    横田伸一, 天野憲一, 西谷千明, 有木茂, 黒木由夫, 藤井暢弘

    エンドトキシン・自然免疫研究15－飛躍する自然免疫研究－   15   1 - 6   2012

    　More details

    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (other)  

    researchmap

  • 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

    　More details

    Language：Japanese   Publisher：医学図書出版(株)  

    Ichushi

    researchmap

  • 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

    　More details

    Language：Japanese   Publisher：医学図書出版(株)  

    Ichushi

    researchmap

  • 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

    　More details

    Language：Japanese   Publisher：医学図書出版(株)  

    Ichushi

    researchmap

  • 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

    　More details

    Language：Japanese   Publisher：日本肺サーファクタント・界面医学会  

    Ichushi

    researchmap

  • 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

    　More details

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

    Ichushi

    researchmap

  • 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

    　More details

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

    Ichushi

    researchmap

  • 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

    　More details

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

    Ichushi

    researchmap

  • 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

    　More details

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

    Web of Science

    researchmap

  • 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 )   2011.3

    　More details

    Language：Japanese   Publisher：社団法人日本泌尿器科学会  

    researchmap

  • 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

    　More details

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

    Web of Science

    researchmap

  • 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

    　More details

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

    Web of Science

    researchmap

  • 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

    　More details

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

    Ichushi

    researchmap

  • 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

    　More details

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

    Ichushi

    researchmap

  • 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

    　More details

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

    Ichushi

    researchmap

  • 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

    　More details

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

    Ichushi

    researchmap

  • 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

    　More details

    Language：Japanese   Publisher：(株)先端医学社  

    肺サーファクタント蛋白質D(SP-D)がLPS受容体であるTLR4-MD-2受容体複合体と結合するか調査し、LPSが惹起するTLR4介在炎症反応に対応するSP-Dの影響と、そのLPSシグナル伝達抑制のメカニズムについてSP-Dの多量体構造に着目し検討した。SP-Dはリガンド、非リガンドに拘わらず、LPS惹起炎症反応を抑えることが明らかになった。その機序としてSP-DはLPSとその受容体との相互作用を変化させることにより炎症性シグナルを抑制することが示された。更に、キメラ体やCRFではLPS惹起炎症反応に対する抑制効果が減弱することからSP-DによるTLR4介在LPSシグナルの抑制機能発現にはSP-Dの十字架多量体構造が重要であることが示唆された。

    Ichushi

    researchmap

  • 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

    　More details

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

    Ichushi

    researchmap

  • 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

    　More details

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

    Ichushi

    researchmap

  • 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

    　More details

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

    Ichushi

    researchmap

  • 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

    　More details

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

    Web of Science

    researchmap

  • 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

    　More details

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

    Web of Science

    researchmap

  • 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

    　More details

    Language：Japanese   Publisher：(株)先端医学社  

    Ichushi

    researchmap

  • 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

    　More details

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

    Ichushi

    researchmap

  • 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

    　More details

    Language：Japanese   Publisher：(一社)日本補体学会  

    Ichushi

    researchmap

  • 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

    　More details

    Language：Japanese   Publisher：(一社)日本補体学会  

    Ichushi

    researchmap

  • 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

    　More details

    Language：Japanese   Publisher：(一社)日本補体学会  

    Ichushi

    researchmap

  • 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

    　More details

    Language：Japanese   Publisher：(一社)日本補体学会  

    Ichushi

    researchmap

  • カブトガニのToll‐like receptorと血液凝固系

    有木茂, 稲森啓一郎, 川畑俊一郎

    臨床免疫   43 ( 2 )   197 - 199   2005.2

    　More details

    Language：Japanese  

    J-GLOBAL

    researchmap

▼display all

Research Projects

  • 感染微生物の排除過程における肺コレクチンの新規生理作用の解明

    Grant number：22K08285  2022.4 - 2025.3

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    有木 茂

    　 More details

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

    researchmap

  • 尿路病原性大腸菌に対する異所性肺コレクチンの生体防御機能の分子基盤解明

    Grant number：17K11185  2017.4 - 2020.3

    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)

    有木 茂

    　 More details

    Authorship：Principal investigator 

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

    今年度は、肺コレクチン（SP-AおよびSP-D）の大腸菌に対する増殖抑制活性が、異なる種類の緩衝液中でどのように変化するのかを詳細に解析した。また、SP-Aのコラーゲン様ドメインとSP-Dの糖鎖認識ドメインを組み合わせたキメラタンパク質を用いて、増殖抑制活性と構造の機能相関を解析した。その結果、カルシウムイオンを含む緩衝液中では、コレクチンが十字架様構造をとっていることが増殖抑制活性に必須であることが明らかとなった。一方、カルシウムイオンを含まない緩衝液中では、コレクチンが花束様構造をとっていることが必須であった。いずれの緩衝液中でも、コレクチンの糖鎖認識ドメインの種類は結果に影響しなかった。これらの結果は、緩衝液の組成が異なることでコレクチンが大腸菌へ結合できなくなることに起因する可能性がある。そこで、大腸菌とコレクチンをそれぞれの緩衝液中で混合した後、大腸菌を遠心により回収して、結合したコレクチンをウエスタンブロッティングにより検出した。その結果、SP-A、SP-D、キメラタンパク質の全てが、いずれの緩衝液中でも大腸菌に結合していた。
    ここまでの結果から、コレクチンの大腸菌に対する増殖抑制活性には、コレクチンの結合特異性よりもオリゴマー構造が重要であると考えられる。そこで、SP-A（花束構造）、SP-D（十字架構造）、キメラタンパク質（花束構造）を混合した場合にどのような効果が得られるのかを解析してみると、予想通り、キメラタンパク質はSP-Aと相加的にはたらいたが、SP-Dの効果は抑制した。
    今年度の解析から、大腸菌に対するコレクチンの構造機能相関をこれまでよりも詳細に明らかにできた。

    researchmap

  • Regulation of ErbB receptors by N-glycans

    Grant number：26440058  2014.4 - 2017.3

    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, ARIKI Shigeru, WADA Yoshinao

    　 More details

    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.

    researchmap

  • 肺コレクチンによるレジオネラ菌の細胞内増殖抑制の分子機構解明

    2014

    秋山記念生命科学振興財団研究助成金（奨励） 

    　 More details

    Authorship：Principal investigator 

    researchmap

  • 抗菌ペプチドによる組織傷害をSP-Aが抑制する分子機構の解明

    2014

    武田科学振興財団医学系研究奨励（基礎） 

    　 More details

  • 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

    　 More details

    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.

    researchmap

  • Studies on molecular basis of inhibitory effect of surfactant protein A against cytotoxicity of human b-defensin3.

    Grant number：24591173  2012.4 - 2015.3

    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)

    ARIKI Shigeru, KUROKI Yoshio, UEHARA Yasuaki

    　 More details

    Authorship：Principal investigator  Grant type：Competitive

    Grant amount：\5330000 （ Direct Cost: \4100000 、 Indirect Cost：\1230000 ）

    Antimicrobial peptides are host defense peptides with a broad spectrum of microbicidal activity. In this study, we suggested that combined use of hBD3 and SP-A-derived peptide (SAP01) is a candidate as a therapeutic reagent against infectious diseases. Binding of SAP01 to hBD3 attenuated cytotoxicity and excess inflammation induced by hBD3. Interestingly, SAP01 did not affect microbicidal activity at concentration sufficient for anti-cytotoxic activity. Because hBD3 also effectively kill drug-resistant microbes, there is appreciable interest in hBD3 for pharmaceutical applications.

    researchmap

  • Studies on host defense mechanisms of pulmonary collectins against Legionella pneumophila.

    Grant number：22790764  2010 - 2011

    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)

    ARIKI Shigeru

    　 More details

    Authorship：Principal investigator  Grant type：Competitive

    Grant amount：\4030000 （ Direct Cost: \3100000 、 Indirect Cost：\930000 ）

    Pulmonary collectins play important roles in innate immunity of the lung. In this study, we found that pulmonary collectins attenuate autophagy induced by L. pneumophila infection. Furthermore, pulmonary collectins inhibit the secretion of effector molecules into host cells via type IV secretion system of L. pneumophila. These results suggest that pulmonary collectins protect host cells by the previously uncharacterized host defense mechanism against intracellular pathogen.

    researchmap

  • Analysis of the interactions of collectins with immunoglobuins and the regulation immunoglobulin functions

    Grant number：20570136  2008 - 2010

    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)

    SHIMIZU Takeyuki, KUROKI Yoshio, NISHITANI Chiaki, ARIKI Shigeru

    　 More details

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

    We found that MBL and SP-D bound to IgM through CRD. The interactions between MBL and IgM in immune complexes depended on the affinity and antigen-density. These results suggest that antigen-bound IgM can take different conformations, which are distinguished by MBL. We also found that MBL can modulate classical pathway of complement cascade.

    researchmap

  • 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)  Grant-in-Aid for Scientific Research (B)

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

    　 More details

    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.

    researchmap

  • Studies on host defense mechanisms of pulmonary collectins against Mycobacterium avium and Legionella pneumophila.

    Grant number：20790574  2008 - 2009

    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)

    ARIKI Shigeru

    　 More details

    Authorship：Principal investigator  Grant type：Competitive

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

    Pulmonary collectins play important roles in innate immunity of the lung. In this study, we demonstrated that collectins prevent the spread of infection by inhibiting the growth of L. pneumophila and M. avium, and by agglutinating M. avium. Furthermore, collectins enhanced the clearance of L. pneumophila by macrophages.

    researchmap

  • 自然免疫におけるリポ多糖認識の分子基盤

    Grant number：05J06104  2005 - 2006

    日本学術振興会  科学研究費助成事業 特別研究員奨励費  特別研究員奨励費

    有木 茂

    　 More details

    Authorship：Principal investigator 

    Grant amount：\1800000 （ Direct Cost: \1800000 ）

    カブトガニの顆粒細胞は、グラム陰性菌のリポ多糖(LPS)に鋭敏に反応し、顆粒内の生体防御蛋白質を体液中へ分泌する。この分泌反応は、細胞質に存在する三量体G蛋白質を介したシグナル伝達によって引き起こされることが推定されていたが、詳細な分子メカニズムは不明なままであった。そこで本研究では、LPS認識およびシグナル伝達に関与する分子の同定を目的として研究を行なった。
    前年度までに、この分泌反応に関与すると考えられるG蛋白質のαサブユニット(Giα)2種類のcDNAクローニングに成功した。これらの分子がLPSシグナルの伝達に関与していること確かめるために、カブトガニ顆粒細胞を用いたRNAi実験系を構築した。実験の結果、2つのGiαのうちのひとつ(Giα1)をノックダウンすると、顆粒細胞のLPSに対する感受性が低下する結果が得られた。
    一方、顆粒細胞表面にはLPSによって活性化されるプロテアーゼ前駆体(C因子)が存在しており、LPS受容体として機能していると考えられている。C因子に対する抗体で顆粒細胞を免疫染色したところ、顆粒細胞の特定の領域がパッチ状に染色された。この結果は、C因子がコレステロールを介してマイクロドメインに結合しているという、これまでの仮説を強く支持するものである。
    前年度に報告したTachyplesinによる顆粒細胞の分泌反応増幅機構を含め、本研究ではカブトガニ顆粒細胞によるリポ多糖認識の分子基盤を解明することができた。

    researchmap

  • カブトガニ顆粒細胞の分泌機構

    2004

    内藤記念特定研究助成金 

    　 More details

    Authorship：Principal investigator 

    researchmap

▼display all

Teaching Experience

  • 化学２

    2017 Institution：札幌医科大学保健医療学部

    　More details

  • 自然科学実験

    2017 Institution：札幌医科大学保健医療学部

    　More details

  • 化学１

    2017 Institution：札幌医科大学保健医療学部

    　More details

  • 自然科学実験

    2015 Institution：札幌医科大学医学部

    　More details

  • 新入生チュートリアル

    2014 Institution：札幌医科大学医学部

    　More details

  • 基礎生化学

    2014 Institution：札幌医科大学医学部

    　More details

  • 生化学

    2011 Institution：札幌医科大学医学部

    　More details

  • 生化学実習

    2007 Institution：札幌医科大学医学部

    　More details

  • PBLチュートリアル

    　More details

▼display all