| Project/Area Number |
24390213
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
INAGI Reiko 東京大学, 医学部附属病院, 特任准教授 (50232509)
WADA Takehiko 東京大学, 医学部附属病院, 講師 (90447409)
TANAKA Tetsuhiro 東京大学, 医学部附属病院, 病院講師 (90508079)
OHSE Takamoto 東京大学, 医学部附属病院, その他 (10568447)
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| Co-Investigator(Renkei-kenkyūsha) |
KODAMA Tatsuhiko 東京大学, 先端科学技術センター, 教授 (90170266)
ABURATANI Hiroyuki 東京大学, 先端科学技術センター, 教授 (10202657)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥18,070,000 (Direct Cost: ¥13,900,000、Indirect Cost: ¥4,170,000)
Fiscal Year 2014: ¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2013: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
Fiscal Year 2012: ¥8,580,000 (Direct Cost: ¥6,600,000、Indirect Cost: ¥1,980,000)
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| Keywords | 低酸素 / HIF / エピジェネティックス / エピゲノム / ヒストン修飾 / 慢性腎臓病 / 腎細胞癌 / エピジェネティクス |
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| Outline of Final Research Achievements |
To elucidate a pathogenic role of epigenetic changes in the kidney in vivo, we tried to optimize experimental conditions to perform ChIP-seq of organs. We attempted to perform PAT-ChIP utilizing laser capture microdissection. However, we could not obtain RNA with the quality high enough for ChIP analysis. We finally decided to perform ChIP of the whole kidney with expectation that the results should reflect change of the tubules, which comprise most of the kidney. We employed a kidney fibrosis model that develops long after transient acute kidney injury by ischemia/reperfusion. We found that fibrotic conditions alter by treatment of compounds that regulate histone modifications.
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