| Project/Area Number |
25340027
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Risk sciences of radiation and chemicals
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| Research Institution | Niigata University |
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Principal Investigator |
OBATA Miki 新潟大学, 医学部, 教務職員 (00420307)
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| Co-Investigator(Kenkyū-buntansha) |
MISHIMA Yukio 新潟大学, 医歯学系, 准教授 (30142029)
KOMINAMI Ryo 新潟大学, 医歯学総合研究科, 研究員 (40133615)
KATSURAGI Yoshinori 新潟大学, 医歯学系, 助教 (60401759)
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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 |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | BCL11B / がん抑制遺伝子 / SWI/SNF複合体 / 放射線応答 / p53-MDM2フィードバックループ / がん抑制因子 / SWI/SNIF複合体 / グリセロール密度勾配遠心法 / DNAチップ解析 |
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| Outline of Final Research Achievements |
Comprehensive profiling of cancer genomics has revealed that somatic mutations of genes encoding SWI/SNF chromatin complexes are a common driver mechanism of tumorigenesis. Since BCL11B was reported to affect transcription as a SWI/SNF component, we examined whether BCL11B incorporated into SWI/SNF complexes in HCT116 cells by transfecting BCL11B expression plasmids into cells, followed by glycerol density sedimentation analysis of the cell lysates. Most of the wild-type BCL11B but not the mutant-type BCL11B proteins were detected in the fractions of large complexes with BRG1 and other SWI/SNF components, indicating that BCL11B is the subunit of SWI/SNF complexes. Initially, we attempted to investigate whether the mutation of BCL11B affects the oscillation of p53-MDM2 by gamma ray irradiation. We failed to detect the difference of oscillation of p53-MDM2 between in the presence of wild-type and mutant-type BCL11B.
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