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Functional analysis of histone variants controlling cell proliferation

Research Project

Project/Area Number 15K14448
Research Category

Grant-in-Aid for Challenging Exploratory Research

Allocation TypeMulti-year Fund
Research Field Molecular biology
Research InstitutionKyoto University

Principal Investigator

Yonehara Shin  京都大学, 生命科学研究科, 教授 (00124503)

Project Period (FY) 2015-04-01 – 2017-03-31
Project Status Completed (Fiscal Year 2016)
Budget Amount *help
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Keywords細胞死 / 細胞増殖 / ヒストンH1 / エピジェネティクス
Outline of Final Research Achievements

FLASH/casp8ap2 is involved in cleavage and maturation of canonical histone mRNA. When the expression of FLASH is suppressed, progression of the cell cycle arrests in the S phase and cell death is induced. At this time, expression of canonical histone H1.4 was shown to be inhibited and expression of non-canonical histone H1t was induced. On the other hand, down-regulated expression of H1.4 in FLASH-expressing cells did not affect cell cycle progression, while cellular proliferation was suppressed by transient expression of exogenous H1t. We consider that the inhibition of cell cycle progression at the S phase by the downregulated expression of FLASH may be due to the expression of H1t, and the new function of H1t on cell cycle progression will be further analyzed by generation and analysis of H1t knockout cells.

Report

(3 results)
  • 2016 Annual Research Report   Final Research Report ( PDF )
  • 2015 Research-status Report
  • Research Products

    (1 results)

All 2016

All Presentation (1 results) (of which Int'l Joint Research: 1 results,  Invited: 1 results)

  • [Presentation] 特異的遺伝子の発現抑制による がん細胞特異的な細胞死の誘導2016

    • Author(s)
      米原 伸
    • Organizer
      第13回東レ先端融合研究シンポジウム
    • Place of Presentation
      東レ先端融合研究所(神奈川県・鎌倉市)
    • Related Report
      2016 Annual Research Report
    • Int'l Joint Research / Invited

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Published: 2015-04-16   Modified: 2018-03-22  

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