Analysis of GADD34 function in aging, nutrient control and wound healing
| Project/Area Number |
22700691
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Applied health science
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| Research Institution | Nagoya University |
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Principal Investigator |
ITO Sachiko 名古屋大学, 医学系研究科, 助教 (70447845)
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| Project Period (FY) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | GADD34 / mTORシグナル / 絶食ストレス / 創傷治癒 / 栄養欠乏ストレス / TORシグナル伝達系 / 老化 / 栄養制御 |
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| Research Abstract |
In this study, we analyzed the function of Growth arrest and DNA damage protein 34 (GADD34) in aging, nutrient deficient-stress and wound healing by using GADD34 Knock out(KO)mice. Starvation induced the expression of GADD34 in the liver. GADD34 bound to and dephosphorylated pTSC2. The dephosphorylation of pTSC2 leads to the suppression of mTOR, which isa potent inhibitor of autophagy. The starvation-induced GADD34 suppressed mTOR and induced autophagy. In wound healing, the rate of wound closure was faster in GADD34 KO MEFs (mouse embryonic fibroblasts) than in wild type(WT) MEFs. WT mice expressed higher amounts of myosin IIA in migrating macrophages and myofibroblasts than in GADD34 KO mice. These results indicate that GADD34 negatively regulates cell migration in wound healing via expression of Myosin IIA.
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Report
(3 results)
Research Products
(14 results)
