| Project/Area Number |
25460291
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General physiology
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| Research Institution | Kagawa University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TOKUDA Masaaki 香川大学, 医学部・細胞情報生理学, 教授 (10163974)
KAMOTORI Kazuyo 香川大学, 医学部・細胞情報生理学, 助教 (40457338)
Dong Youyi 香川大学, 医学部・細胞情報生理学, 助教 (90457341)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | S100 proteins / Helix repeat proteins / protein phoshatase 5 / beta catenin / cdc-37 / S00蛋白質 / PP5 / βカテニン / cdc37 / HSP90 / S100蛋白質 / BCL9 / Hsp90 |
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| Outline of Final Research Achievements |
S100A2 and S100A6 bound to the first armadillo repeat of beta-catenin and inhibited the beta-catenin-BCL9 interaction. Over-expression of S100A6 in KEK293 cells inhibited the transcriptional activity of TCF4. Knocking down of S100A6 in HCT116 and HT29 increased the cyclin D1 expression. And over-expression of S100A6 inhibited the cell growth.
S100A2, A2, and A6 inhibited the Hsp90/PP5/cdc-37 complex formation and inhibited the dephosphorylation of cdc-37 protein in vitro. Over-expression of these S100 proteins in COS7 cells also inhibited the cdc-37 dephosphorylation that could influence the maturation of client proteins of cdc37.
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