| Project/Area Number |
24790196
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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 |
General anatomy (including Histology/Embryology)
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| Research Institution | Yamaguchi University |
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Principal Investigator |
FUJINAGA Ryutaro 山口大学, 医学(系)研究科(研究院), 講師 (30335723)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2013: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | HAP1 / stigmoid body / ストレス / 細胞分裂 / ハンチントン病 / アポトーシス / プロテアソーム |
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| Research Abstract |
Huntingtin-associated protein 1 is a core molecule of the cytoplasmic inclusion, stigmoid body (STB). First, we examined cell-cycle dependent change in HAP1 distribution in HAP1-transfected HeLa cells. In interphase, HAP1 formed large-sized STBs. During mitosis, most of the HAP1/STB disappeared but a subset of HAP1 was concentrated at the spindle poles. When cells entered cytokinesis, HAP1 started to form small-sized STB-like inclusion. Next, we examined effect of stress exposures on HAP1/STB morphology in HAP1-transfected immortalized mouse hypothalamic cell line. HAP1 formed typical STBs in most of the stress conditions (e.g., heat shock, ER stress and serum-starvation). However, in proteasome inhibited condition, HAP1 induced cytoplasmic glanulo-reticular clusters instead of STB formation. Now we are analyzing the mechanism of change in HAP1/STB morphology and its biological significance in proteasome-inhibitor-induced apoptosis.
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