| Project/Area Number |
26450408
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Veterinary medical science
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| Research Institution | Osaka Prefecture University |
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Principal Investigator |
Nakagawa Hiroshi 大阪府立大学, 生命環境科学研究科, 助教 (60336807)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2016: ¥520,000 (Direct Cost: ¥400,000、Indirect Cost: ¥120,000)
Fiscal Year 2015: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | ER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 / 細胞毒性 / 細胞内輸送 |
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| 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.
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