Mechanisms maintaining neuronal survival via necdin-centered protein interaction networks
| Project/Area Number |
21300138
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurochemistry/Neuropharmacology
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| Research Institution | Osaka University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
OHKUMO Tsuyoshi 大阪大学, 蛋白質研究所, 助教 (50432505)
HASEGAWA Koichi 大阪大学, 蛋白質研究所, 助教 (20546783)
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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 |
¥18,590,000 (Direct Cost: ¥14,300,000、Indirect Cost: ¥4,290,000)
Fiscal Year 2011: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
Fiscal Year 2010: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
Fiscal Year 2009: ¥6,630,000 (Direct Cost: ¥5,100,000、Indirect Cost: ¥1,530,000)
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| Keywords | Necdin / 蛋白質ネットワーク / Sirt1 / Fox01 / SMC5/ 6複合体 / エネルギー代謝 / DNA修復 / 哺乳類ニューロン / FoxO1 / SMC5/6複合体 / 視床下部 / Sirtl / FoxOl / アセチル化 / SMC5 / 6複合体 / NSE3 |
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| Research Abstract |
Necdin interacted with Sirt1, which deacetylates various energy metabolism-associated proteins, and controlled the acetylation levels of the Fox01 transcription factor and neuropeptidergic neuron activities in the hypothalamus. Necdin also interacted with several elements of the SMC5/ 6 complex, which is involved in DNA repair, and enhanced its activity after DNA damage in postmitotic neurons. These results suggest that necdin serves as a hub protein in the protein interaction networks that are involved in energy metabolism and DNA repair to promote neuronal survival.
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Report
(4 results)
Research Products
(41 results)
