| Project/Area Number |
12670106
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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 | Kanazawa University |
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Principal Investigator |
ITO Takashi Kanazawa Univ., Cancer Res. Inst., Professor, がん研究所, 教授 (90201326)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2001: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | GCN1 / GCN2 / YIH1 / autophagy / GIドメイン / 翻訳制御 |
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| Research Abstract |
The yeast Impact homolog YIH1 competes with the eIF2oc kinase GCN2 for GCN 1 -binding, because both share GI domain interacting with GCN1. The GI domain-mediated association of GCN2 with GCN1 is essential for the activation of eIF2a kinase activity of GCN2 and hence for stress response to amino acid starvation (general control response). We also found evidence for a crosstalk between general control reponse and the target of rapamycin (TOR) signaling pathways. Intriguingly, TOR and GCN2 have been shown to regulate autophagy and YIH1 was identified as a regulator of autophagy of nuclei. These results suggest that a molecular network contaning TOR, GCN2 and YIH 1 setms to regulate autophagy.
For mouse Impact, we started gene-targeting and one-hybrid screening for the factors interacting with the differentially methylted region in this gene. We also found HRH4/Hrh4 gene adjacent to IMPACT/Impact escape imprinting.
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