The Roles of HSF2 Complex in Huntington's disease mice.
Project/Area Number |
25430090
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Laboratory animal science
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Research Institution | Yamaguchi University |
Principal Investigator |
HAYASHIDA Naoki 山口大学, 医学(系)研究科(研究院), 講師 (40420517)
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Project Period (FY) |
2013-04-01 – 2016-03-31
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Project Status |
Completed (Fiscal Year 2015)
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Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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Keywords | HSF2 / Set1/MLL 複合体 / H3K4 / alphaB-クリスタリン / プロモーター / メチル化 / 遺伝子活性化 / ハンチントン病マウス / 疾患モデルマウス / HeLa細胞 / 神経芽細胞 / Neuro-2a / 増殖 / 転写因子 / WDR5 / Set1/MLL / H3K4メチル化 / 変性タンパク質 / トランスジェニックマウス / ハンチントン病 / 熱ショック因子 / ヒストン修飾 / クロマチン / ヒストンメチル化酵素 / CRYAB |
Outline of Final Research Achievements |
We discovered the novel functions of HSF2. We already published a few data in Hayashida, BBRC 2015. We also discovered Se1/MLL complex, this complex is methylates H3K4 and avtivates many genes, binds to HSF2. We previously used Huntington's disease model mice and found alphaB-crystallin (CRYAB) is important, therefore, we analyzed the CRYAB promoter. HSF2 and Set1/MLL complex bound to the promoter under both normal and heta-stressed conditions. However, the binding of Set1/MLL complex depends on HSF2. We already HSF2 is critical factor in the survival of Huntington's mice (Shinkawa, Hayashida et al., MBC 2011), This time, we successfully reveraled the novel mechanism why the life span of Huntington's disease mice become prominently shortened.
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Report
(4 results)
Research Products
(27 results)
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[Journal Article] Mitochondrial SSBP1 protects cells from proteotoxic stresses by potentiating stress-induced HSF1 transcriptional activity.2015
Author(s)
Tan, K., Fujimoto, M., Takii, R., Takaki, E., Hayashida, N., Nakai, A.
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Journal Title
Nature Communications
Volume: 6
Issue: 1
Pages: 6580-6594
DOI
NAID
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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