2017 Fiscal Year Final Research Report
Elucidation of the regulatory mechanisms of aging using senescence-accerelation mice
| Project/Area Number |
16K15239
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pathological medical chemistry
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Keywords | 細胞老化 |
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| Outline of Final Research Achievements |
In order to clarify whether acceleration of cellular senescence enhances age-related changes in vivo and shorten the lifespan, we generated senescence acceleration mice using non-degradation mutant of Claspin. Mouse embryonic fibroblasts from transgenic mice harboring non-degradation mutant of Claspin (Senescence acceleration mice) showed a significant higher sensitivity to senescence upon low level of genome stresses than those from wild-type mice. Interestingly, the senescence acceleration mice exhibited acceleration of some age-associated phenotypes such as emaciation, lordokyphosis, and inactive. These results thus suggest that high senescence sensitivity accelerates aging phenotypes in vivo.
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| Free Research Field |
分子腫瘍学
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