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2016 Fiscal Year Final Research Report

Involvement of rER localized trimeric G protein in inhibitory regulation of protein transport in ER stress

Research Project

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Project/Area Number 26450408
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Veterinary medical science
Research InstitutionOsaka Prefecture University

Principal Investigator

Nakagawa Hiroshi  大阪府立大学, 生命環境科学研究科, 助教 (60336807)

Project Period (FY) 2014-04-01 – 2017-03-31
KeywordsERストレス / 細胞内小胞輸送 / アポトーシス / 三量体Gタンパク
Outline of Final Research Achievements

Although it was expected that existence of ER to Golgi protein transport regulatory system in ER stress induced cells, regulation of ER to Golgi protein transport remained unclear. Since rER membrane localized trimeric Gi2 protein regulated ER to Golgi protein transport, we examined relationship between ER stress responses and rER membrane localized trimeric G protein.
Knockdown of trimeric Gi2 protein suppressed ER stress. Although PERK was activated in ER stress, knockdown of trimeric Gi2 protein inhibited CHOP activation, downstream signal molecule of PERK. Furthermore, knockdown of Gi2 protein inhibited ATF6 activation. This results suggests that rER membrane localized trimeric G protein involves in ER stress response. Thus, we conclude that rER membrane localized trimeric G protein is a new target of apoptosis regulation.

Free Research Field

トキシコロジー

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Published: 2018-03-22  

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