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Retinal phosphoprotein analysis in novel Src mutant optic neuropathy mouse model

Research Project

Project/Area Number 25670729
Research Category

Grant-in-Aid for Challenging Exploratory Research

Allocation TypeMulti-year Fund
Research Field Ophthalmology
Research InstitutionUniversity of Yamanashi

Principal Investigator

KATO Goro  山梨大学, 総合研究部, 助教 (60177441)

Project Period (FY) 2013-04-01 – 2015-03-31
Project Status Completed (Fiscal Year 2014)
Budget Amount *help
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Keywords網膜 / Src / リン酸化タンパク質 / Srcセリン75リン酸化 / Src / 網膜神経細胞 / タンパク質リン酸化
Outline of Final Research Achievements

Degradation of activated Src is regulated by Cdk5-dependent phosphorylation of Src Ser75. RGC loss was stimulated without elevated intraocular pressure in the aged phospho-mimicking mutant SrcSer75Asp mice (SD mice).To address the molecular mechanism of the degeneration induced by deregulation of the Ser75 phosphorylation, we established 2-D Fluorescence Difference Gel Electrophoresis (2-D DIGE) to globally detect changes in the retinal phosphoprotein abundance in retinas. The level of spot #30, which had an apparent molecular weight of 45kDa and an isoelectric point of 5.5~6.5, in SD mice was increased significantly than that of wild type mice.These results can lead to identification of retinal phosphoproteins changed by the Src-specific phosphorylation mutation, and are very important in elucidating the mechanism of RGC degeneration.

Report

(3 results)
  • 2014 Annual Research Report   Final Research Report ( PDF )
  • 2013 Research-status Report
  • Research Products

    (1 results)

All Other

All Remarks (1 results)

  • [Remarks] 山梨大学研究者総覧

    • Related Report
      2013 Research-status Report

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Published: 2014-07-25   Modified: 2019-07-29  

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