| Project/Area Number |
23700512
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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 |
Laboratory animal science
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| Research Institution | Yamaguchi University |
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Principal Investigator |
HAYASHIDA Naoki 山口大学, 大学院・医学系研究科, 講師 (40420517)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 熱ショック因子 / 転写 / 神経変性疾患 / H3K4トリメチル化 / クロマチン / プロモーター / HSF1 / ポリグルタミン病 / 熱ショック転写因子 / HSF2 / ハンチントン病 / 蛋白質分解 / ヒストンメチル化 / 細胞防御 |
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| Research Abstract |
The heat shock transcription factor (heat shock factor) HSF2 is an important HSF for cortical development and highly-expressed in CNS, however, whether it can suppress cellular stress and denatured protein-mediated toxicity causing neurodegenerative diseases or not. By the support of this grand-in-aid, the principal investigator revealed that HSF2 can suppress the intracellular aggregation caused by denatured or unfolded protein. We also analyzed the novel mechanism of HSF2-mediated cytoprotection. Although only HSF1 has chromatin opening and transcription activating ability among four HSFs, some of these novel HSF2 target genes were activated by HSF2 alone in the HSF1-deficient cells. These results suggest that HSF2 has the chromatin opening activity as well as HSF1, and that the induction of novel HSF2 regulated genes involved in toxic protein degradation can lead to the suppression of neurodegenerative diseases.
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