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2017 Fiscal Year Final Research Report

Elucidation and application of regulatory mechanisms underlying biogenesis of transport vesicles budding from the endoplasmic reticulum

Research Project

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Project/Area Number 15K07384
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Applied biochemistry
Research InstitutionNagoya University

Principal Investigator

Shibata Hideki  名古屋大学, 生命農学研究科, 准教授 (30314470)

Co-Investigator(Renkei-kenkyūsha) MAKI Masatoshi  名古屋大学, 大学院生命農学研究科, 教授 (40183610)
TAKAHARA Terunao  名古屋大学, 大学院生命農学研究科, 助教 (90708059)
Research Collaborator KUWATA Keiko  名古屋大学, トランスフォーマティブ生命分子研究所, 特任助教 (70624352)
KANADOME Takashi  名古屋大学, 大学院生命農学研究科, 大学院生
SATO Akane  名古屋大学, 大学院生命農学研究科, 大学院生
INOUE Kuniko  名古屋大学, 大学院生命農学研究科, 大学院生
ARAI Yumika  名古屋大学, 大学院生命農学研究科, 大学院生
KONO Yuta  名古屋大学, 大学院生命農学研究科, 大学院生
Project Period (FY) 2015-04-01 – 2018-03-31
Keywordsカルシウム / COPII小胞 / 分泌経路 / タンパク質間相互作用 / 小胞体
Outline of Final Research Achievements

In mammalian cells, proteins destined for secretion are transported from specialized region of the ER, called ER exit site (ERES), by COPII vesicles. The aim of this study was to investigate the role of ALG-2, a calcium-binding protein, in the regulation of COPII-mediated protein transport. ALG-2 directly interacts with Sec31A, an outer coat component of COPII. Firstly, we identified Trk-fused gene (TFG) product as a novel target for ALG-2. Overexpression of ALG-2 enhanced the localization of TFG to the ERES. Secondly, MISSL was shown to be recruited to the ERES by ALG-2 in response to calcium mobilization. We also found that ALG-2 bridged between MISSL and MAP1B. In our co-immunoprecipitation analysis, TFG, MISSL and MAP1B did not form the complex with Sec31A, suggesting that ALG-2 may have divergent functions at the ERES. Finally, we reported that amyotrophic lateral sclerosis (ALS)-associated mutations in annexin A11 caused abnonormality in binding to S100A6.

Free Research Field

応用生物化学

URL: 

Published: 2019-03-29  

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