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Transcriptional regulation of a novel BTB-zinc finger protein GetB (CIBZ)

Research Project

Project/Area Number 16590230
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field General medical chemistry
Research InstitutionNara Institute of Science and Technology

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)

Project Period (FY) 2004 – 2005
Project Status Completed (Fiscal Year 2005)
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)
KeywordsTranscription / 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
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.

Report

(3 results)
  • 2005 Annual Research Report   Final Research Report Summary
  • 2004 Annual Research Report
  • Research Products

    (3 results)

All 2005 2004

All Journal Article (3 results)

  • [Journal Article] Identification of a novel BTB-zinc finger transcriptional repressor, CIBZ, that interacts with CtBP corepressor2005

    • Author(s)
      Eishou Matsuda, Nobuhiro Sasai, Eimiko Sarashina, Yasumasa Ishida, Masashi Kawaichi
    • Journal Title

      Genes to Cells 10

      Pages: 871-885

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2005 Annual Research Report 2005 Final Research Report Summary
  • [Journal Article] Identification of a novel BTB-zinc finger transcriptional repressor, CIBZ, that interacts with CtBP corepressor2005

    • Author(s)
      Eishou Matsuda, Nobuhiro Sasai, Eimiko Sarashina, Yasumasa Ishida, Masashi Kawaichi
    • Journal Title

      Genes to Cells 10(9)

      Pages: 871-885

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2005 Final Research Report Summary
  • [Journal Article] Expression profiling with arrays of randomly disrupted genes in mouse embryonic stem cells leads to in vivo functional analysis2004

    • Author(s)
      Eishoo, Matsuda
    • Journal Title

      Proceeding of the National Academy of Science of the United States of America 10

      Pages: 1073-1073

    • Related Report
      2004 Annual Research Report

URL: 

Published: 2004-04-01   Modified: 2016-04-21  

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