Role and mechanism of action of mammalian Elongin A in the stress response
| Project/Area Number |
21590311
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General medical chemistry
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| Research Institution | Kochi University |
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Principal Investigator |
ASO Teijiro 高知大学, 教育研究部・医療学系, 教授 (20291289)
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| Co-Investigator(Renkei-kenkyūsha) |
KITAJIMA Shigetaka 東京医科歯科大学, 難治疾患研究所, 教授 (30186241)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | Elongin / 転写伸長因子 / ユビキチンリガーゼ / ストレス応答 / 発現制御 / RNAポリメラーゼII / RANポリメラーゼII / ストレス |
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| Research Abstract |
Elongin A increases the rate of RNA polymerase II(pol II) transcript elongation by suppressing transient pausing by the enzyme. Elongin A also acts as a component of a ubiquitin ligase(E3) that can target stalled pol II for ubiquitylation and proteasome. dependent degradation. It is not known whether these activities of Elongin A are functionally interdependent in vivo. Here, we demonstrate that Elongin A-knockdown cells exhibit defects in the stress-inducible expression of HSP70 and ATF3 genes. Moreover, we identify Elongin A mutations that selectively inactivate one or the other of the above activities, and show that the elongation stimulatory, but not pol II ubiquitylation, activity of Elongin A is required to support the response of stress genes.
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Report
(4 results)
Research Products
(11 results)
