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Regulation of MUTYH expression by p53 plays a critical role in cell death

Research Project

Project/Area Number 22501014
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Tumor biology
Research InstitutionKyushu University

Principal Investigator

OKA Sugako  九州大学, 生体防御医学研究所, 特任助教 (80467894)

Co-Investigator(Kenkyū-buntansha) NAKABEPPU Yusaku  九州大学, 生体防御医学研究所, 教授 (30180350)
Project Period (FY) 2010 – 2012
Project Status Completed (Fiscal Year 2012)
Budget Amount *help
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Keywordsシグナル伝達と遺伝子発現 / ゲノム / 酸化ストレス / シグナル伝達 / がん / 細胞死 / 癌 / ストレス
Research Abstract

MUTYH, adenine DNA glycosylase excises adenine inserted opposite 8-oxoguanine (8-oxoG), a major form of spontaneous oxidative DNA damage, and whose deficiency is known to cause MUTYH-associated familial adenomatous polyposis. We have shown that accumulation of 8-oxoG in nuclear and mitochondrial DNA independently triggers two distinct MUTYH-dependent cell death programs. In the present study, we found that expression of MUTYH is regulated by p53 and identified functional p53-binding site in MUTYH gene. These results suggest that MUTYH is a potential mediator of p53 tumor suppression.

Report

(4 results)
  • 2012 Annual Research Report   Final Research Report ( PDF )
  • 2011 Annual Research Report
  • 2010 Annual Research Report
  • Research Products

    (18 results)

All 2012 2011 2010 Other

All Journal Article (4 results) (of which Peer Reviewed: 4 results) Presentation (14 results)

  • [Journal Article] 8-Oxoguanine causes neurodegeneration during Mutyh-mediated DNA base excision repair2012

    • Author(s)
      Sheng Z, Oka S, Tsuchimoto D, Abolhassani N, Nomaru H, Sakumi K, Yamada H, Nakabeppu Y
    • Journal Title

      J Clin Invest

      Volume: 12 Pages: 4344-4361

    • Related Report
      2012 Final Research Report
    • Peer Reviewed
  • [Journal Article] MutT Homolog-1 Attenuates Oxidative DNA Damage and Delays Photoreceptor Cell Death in Inherited Retinal Degeneration2012

    • Author(s)
      Murakami Y, Ikeda Y, Yoshida N, Notomi S, Hisatomi T, Oka S, De Luca G, Yonemitsu Y, Bignami M, Nakabeppu Y, Ishibashi T
    • Journal Title

      Am J Pathol

      Volume: 181(4) Pages: 1378-86

    • Related Report
      2012 Final Research Report
    • Peer Reviewed
  • [Journal Article] DNA glycosylase encoded by MUTYH functions as a molecular switch for programmed cell death under oxidative stress to suppress tumorigenesis2011

    • Author(s)
      Oka S, Nakabeppu Y
    • Journal Title

      Cancer Sci

      Volume: 102 Issue: 4 Pages: 677-682

    • DOI

      10.1111/j.1349-7006.2011.01869.x

    • NAID

      10029291748

    • Related Report
      2012 Final Research Report 2011 Annual Research Report
    • Peer Reviewed
  • [Journal Article] DNA Polymerases as Potential Therapeutic Targets for Cancers Deficient in the DNA Mismatch Repair Proteins MSH2 or MLH1

    • Author(s)
      Sarah A. Martin, Nuala McCabe, Michelle Mullarkey, Robert Cummins, Darren J. Burgess, Y Nakabeppu, S Oka, Elaine Kay, Christopher J. Lord and Alan Ashworth
    • Journal Title

      Cancer Cell

      Volume: 17 Pages: 235-245

    • Related Report
      2012 Final Research Report
    • Peer Reviewed
  • [Presentation] MUTYH is a potential mediator of p53 tumor suppression2012

    • Author(s)
      Sugako Oka, Julio Leon, Daisuke Tsuchimoto, Kunihiko Sakumi, Yusaku Nakabeppu
    • Organizer
      第35回日本がん疫学 分子疫学学会
    • Year and Date
      2012-07-05
    • Related Report
      2012 Final Research Report
  • [Presentation] MUTYH is a potential mediator of p53 tumor suppression2012

    • Author(s)
      岡 素雅子
    • Organizer
      第35回日本がん疫学 分子疫学学会
    • Place of Presentation
      広島
    • Related Report
      2012 Annual Research Report
  • [Presentation] MUTYH is a potential mediator of p53 tumor suppression2011

    • Author(s)
      Sugako Oka, Julio Leon, Yusaku Nakabeppu
    • Organizer
      第34回日本分子生物学会
    • Place of Presentation
      横浜
    • Year and Date
      2011-12-14
    • Related Report
      2012 Final Research Report
  • [Presentation] MUTYH is a potential mediator of p53 tumor suppression2011

    • Author(s)
      Sugako Oka, Julio Leon, Yusaku Nakabeppu
    • Organizer
      第34回日本分子生物学会口頭、ポスター
    • Place of Presentation
      横浜
    • Year and Date
      2011-12-14
    • Related Report
      2011 Annual Research Report
  • [Presentation] MUTYH is a potential mediator of p53 tumor suppression2011

    • Author(s)
      Sugako Oka, Julio Leon, Kunihiko Sakumi, Daisuke Tsuchimoto, Yusaku Nakabeppu
    • Organizer
      日本環境変異原学会第40回大会 (シンポジウム)
    • Place of Presentation
      東京
    • Year and Date
      2011-11-21
    • Related Report
      2012 Final Research Report
  • [Presentation] MUTYH is a potential mediator of p53 tumor suppression2011

    • Author(s)
      Sugako Oka, Julio Leon, Kunihiko Sakumi, Daisuke Tsuchimoto, Yusaku Nakabeppu
    • Organizer
      日本環境変異原学会第40回大会シンポジウム発表
    • Place of Presentation
      東京一橋記念講堂
    • Year and Date
      2011-11-21
    • Related Report
      2011 Annual Research Report
  • [Presentation] MUTYH-initiated base excision repair triggers two distinct cell death pathways by monitoring 8-oxoguanine in nuclear and mitochondrial DNAsKeystone Symposia Stem Cells2011

    • Author(s)
      Sugako Oka, Yusaku Nakabeppu
    • Organizer
      Cancer and Metastasis
    • Place of Presentation
      USA
    • Year and Date
      2011-03-08
    • Related Report
      2012 Final Research Report
  • [Presentation] MUTYH-initiated base excision repair triggers two distinct cell death pathways by monitoring 8-oxoguanine in nuclear and mitochondrial DNAs2011

    • Author(s)
      Sugako Oka
    • Organizer
      Keystone Symposia Stem Cells, Cancer and Metastasis
    • Place of Presentation
      Keystone, CO, USA
    • Year and Date
      2011-03-08
    • Related Report
      2010 Annual Research Report
  • [Presentation] MUTYHはp53による発がん抑制のメディエータである2010

    • Author(s)
      岡 素雅子、レオン フリオ、中別府雄作
    • Organizer
      第33回日本分子生物学会年会・第83回日本生化学会大会合同大会
    • Place of Presentation
      神戸
    • Year and Date
      2010-12-09
    • Related Report
      2012 Final Research Report
  • [Presentation] MUTYH-initiated base excision repair triggers two distinct cell death pathways by monitoring 8-oxoguanine in nuclear and mitochondrial DNAs2010

    • Author(s)
      Sugako Oka, Julio Leon, Yusaku Nakabeppu
    • Organizer
      国際3R会議
    • Place of Presentation
      富山
    • Year and Date
      2010-10-27
    • Related Report
      2012 Final Research Report
  • [Presentation] MUTYH-initiated base excision repair triggers two distinct cell death pathways by monitoring 8-oxoguanine in nuclear and mitochondrial DNAs2010

    • Author(s)
      Sugako Oka
    • Organizer
      進化する国際3R会議
    • Place of Presentation
      富山,富山国際会議場(ポスター)
    • Year and Date
      2010-10-27
    • Related Report
      2010 Annual Research Report
  • [Presentation] MUTYH is a potential mediator of p53 tumor suppression2010

    • Author(s)
      Sugako Oka
    • Organizer
      第69回日本癌学会学術総会
    • Place of Presentation
      大阪,大阪国際会議場(ポスター)
    • Year and Date
      2010-09-23
    • Related Report
      2010 Annual Research Report
  • [Presentation] MUTYH is a potential mediator of p53 tumor suppression2010

    • Author(s)
      Sugako Oka, Yusaku Nakabeppu
    • Organizer
      第69回日本癌学会
    • Place of Presentation
      大阪
    • Year and Date
      2010-09-22
    • Related Report
      2012 Final Research Report
  • [Presentation] MUTYHはp53による発がん抑制のメディエータである2010

    • Author(s)
      岡素雅子
    • Organizer
      第33回日本分子生物学会年会・第83回日本生化学会大会 合同大会
    • Place of Presentation
      神戸ポートピアアイランド(ポスター 口頭発表)
    • Related Report
      2010 Annual Research Report

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Published: 2010-08-23   Modified: 2019-07-29  

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