| Project/Area Number |
16590230
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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 | Nara Institute of Science and Technology |
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Principal Investigator |
MATSUDA Eishou Nara Institute of Science and Technology, Biological Sciences, Asst. Prof., バイオサイエンス研究科, 助手 (00335481)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2005: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2004: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | Transcription / BTB domain / Co-repressor / CtBP / Pericentromeric heterochromatin / HDACs / Sumoylation / Methylation / BTB ドメイン / CtBP (C-terminal binding protein of E1A) / HDAC (Histone deacetylase) / TSA / SUMO (small ubiquitin-related modifier) / PIAS (protein inhibitor of activated STAT) / ノックアウトマウス |
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| Research Abstract |
The transcriptional corepressor C-terminal binding protein (CtBP) is thought to be involved in development and oncogenesis, but the regulation of its corepressor activity is largely unknown. We show here that a novel BTB-zinc finger protein, CIBZ (CtBP-interacting BTB zinc finger protein), redistributes CtBP to pericentromeric foci from a diffuse nuclear localization in interphase cells. CIBZ physically associates with CtBP via a conserved CtBP binding motif, PLDLR. When heterologously targeted to DNA CIBZ represses transcription via two independent repression domains, an N-terminal BTB domain and a PLDLR motif-containing RD2 region, in a histone deacetylase-independent and -dependent manner, respectively. Mutation in the PLDLR motif abolishes the CIBZ-CtBP interaction and transcriptional repression activity of RD2, but does not affect the repression activity of the BTB domain. Furthermore, this PLDLR-mutated CIBZ cannot target CtBP to pericentromeric foci, although it is localized to the pericentromeric foci itself. These results suggest that at least one repression mechanism mediated by CIBZ is recruitment of the CtBP/HDAC complex to perioentromeric foci, and that CIBZ may regulate pericentromeric targeting of CtBP.
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