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study of molecular mechanism of catechin on degradative effect of growth factor receptor and suppressive effect of tumor growth

Research Project

Project/Area Number 22890074
Research Category

Grant-in-Aid for Research Activity Start-up

Allocation TypeSingle-year Grants
Research Field Surgical dentistry
Research InstitutionUniversity of Fukui

Principal Investigator

YOSHIMURA Hitoshi  福井大学, 医学部, 助教 (40362917)

Project Period (FY) 2010 – 2011
Project Status Completed (Fiscal Year 2011)
Budget Amount *help
¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
Fiscal Year 2011: ¥1,417,000 (Direct Cost: ¥1,090,000、Indirect Cost: ¥327,000)
Fiscal Year 2010: ¥1,443,000 (Direct Cost: ¥1,110,000、Indirect Cost: ¥333,000)
Keywords癌 / シグナル伝達 / 蛋白質
Research Abstract

Pletelet derived growth factor receptor(PDGFR) is one of the molecule target for cancer treatment. Cathechin has an anti-tumor effect, and we examined the effect for PDGFR. PDGFR protein was decreased by EGCG treatment. The decrease was promoted by the inhibitor of protein synthesis, and suppressed by the inhibitor of protein degradation. PDGFR ubiquitinization was observed by the treatment with EGCG and inhibitor of protein degradation. It was suggested that PDGFR protein was decrease by EGCG treatment through the activation of ubiquitin-proteasome pathway.

Report

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

    (2 results)

All 2010

All Presentation (2 results)

  • [Presentation] エピガロカテキン-3-ガレートによる血小板由来増殖因子受容体分解作用に関する検討2010

    • Author(s)
      吉村仁志
    • Organizer
      第55回日本口腔外科学会総会・学術大会
    • Place of Presentation
      千葉県
    • Year and Date
      2010-10-16
    • Related Report
      2010 Annual Research Report
  • [Presentation] エピガロカテキン-3-ガレートによる血小板由来増殖因子受容体分解作用に関する検討2010

    • Author(s)
      吉村仁志,飛田尚慶,植野高章,関根浄治,佐野和生
    • Organizer
      第55回社団法人日本口腔外科学会総会・学術大会
    • Related Report
      2011 Final Research Report

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Published: 2010-08-27   Modified: 2016-04-21  

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