| Project/Area Number |
23310036
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Risk sciences of radiation/Chemicals
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| Research Institution | Niigata University |
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Principal Investigator |
KOMINAMI Ryo 新潟大学, 医歯(薬)学総合研究科, 客員研究員 (40133615)
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| Co-Investigator(Kenkyū-buntansha) |
MISHIMA Yukio 新潟大学, 医歯学系, 准教授 (30142029)
KATSURAGI Yoshinori 新潟大学, 医歯学系, 助教 (60401759)
OBATA Miki 新潟大学, 医歯学系, 教務職員 (00420307)
広瀬 哲史 (廣瀬 哲史) 新潟大学, 医歯学系, 助教 (10415276)
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| Project Period (FY) |
2011-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥19,630,000 (Direct Cost: ¥15,100,000、Indirect Cost: ¥4,530,000)
Fiscal Year 2013: ¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2012: ¥7,540,000 (Direct Cost: ¥5,800,000、Indirect Cost: ¥1,740,000)
Fiscal Year 2011: ¥8,320,000 (Direct Cost: ¥6,400,000、Indirect Cost: ¥1,920,000)
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| Keywords | 電離放射線 / 発がん / 幹細胞 / 大腸がん / 胸腺リンパ腫 / Bcl11b / Bcl11ｂ / 放射線標的細胞 / 発がん母細胞 / 細胞の増殖と消失 / 腸管腫瘍 |
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| Research Abstract |
Attenuated expression of Bcl11b in Lgr5-expressing intestinal crypt cells promoted regeneration of intestinal epithelial cells after the radiation-induced injury in Lgr5-Cre; Bcl11bflox/+ mice. This suggests that the origin of cells in intestinal tumors, which are enhanced by loss of one Bcl11b allele in Apcmin/+ mice, is Lgr5-expressing cells. It was also demonstrated that Bcl11b functions as a subunit of SWI/SNF chromatin remodeling complex and down-regulates transcription of Wnt/beta-catenin target genes such as c-jun. This suggests that Bcl11b impairment instigates intestinal tumor development at least in part through deregulation of beta-catenin pathway.
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