The molecular mechanism of asymmetric inheritance of damaged proteins.
| Project/Area Number |
25840080
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Cell biology
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| Research Institution | The Institute of Physical and Chemical Research |
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Principal Investigator |
SUZUKI Genjiro 独立行政法人理化学研究所, 脳科学総合研究センター, 研究員 (60466034)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2014: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 細胞老化 / プリオン / 老化 / 酵母 / タンパク質 |
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| Outline of Final Research Achievements |
To elucidate the molecular mechanism of cellular aging, I focused on Mlp proteins and investigated the molecular mechanism of asymmetric inheritance of damaged protein aggregates. I found the mlp mutant strain of budding yeast showed defects in asymmetric inheritance of damaged protein aggregates and prion propagons and shorter life span. I also found Mlp proteins co-localized with damaged protein aggregates. Thus, Mlp proteins must be scaffolds of aggregated proteins in mother cells and retain these aggregates in mother cells to keep the daughter cells fresh.
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Report
(3 results)
Research Products
(4 results)
