2012 Fiscal Year Final Research Report
Analysis of mouse teeth hyperplasia and gut tissue enlargement by mutation of transcription factor Bcl11b
| Project/Area Number |
22592062
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Functional basic dentistry
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| Research Institution | Niigata University |
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Principal Investigator |
MISHIMA Yukio 新潟大学, 医歯学系, 准教授 (30142029)
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| Co-Investigator(Kenkyū-buntansha) |
OBATA Miki 新潟大学, 医学部, 教務職員 (00420307)
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| Project Period (FY) |
2010 – 2012
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| Keywords | 過剰歯形成 / 腸管組織の肥厚 / 転写因子Bcl11b/BCL11B / p^53 / Mdm2/HDM2 |
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| Research Abstract |
Bcl11b/BCL11B is a C_2H_2 zinc finger transcription factor that acts as a haploinsufficient tumor suppressor. Mutations and deletion in the human orthologue BCL11B have been identified in human T-cell acute lymphoblastic leukemia (T-ALL) and a mouse model of thymic lymphomas. We have examined whether or not BCL11B directly affects the p^53 signaling pathway including HDM2, an ubiquitin ligase for p^53 degradation. This is because that the p^53 pathway regulates cell proliferation and the response to DNA damages to maintain genome integrity. We have obtained the results that BCL11B binds to human HDM2-P2 promoter by ChIP (chromatin immuno-precipitation) assay and inhibits HDM2 expression in a p^53-dependent manner. These date suggest that BCL11B affects the activity of the p53-HDM2 feedback loop. This may be a mechanism for the leukemic transformation in T-ALL and for the impairment of incisor development and the enlargement of intestine crypts in Bcl11b S826G/KO mouse.
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[Journal Article] Clonally expanding thymocytes having lineage capability in γ-ray induced mouse atrophic thymus2010
Author(s)
T. Yamamoto, S. Morita, E. Go, M. Obata, Y. Katsuragi, Y. Fujita, Y. Maeda, M. Yokoyama, Y. Aoyagi, H. Ichikawa, Y. Mishima and R. Kominami
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Journal Title
International Journal of Radiation Oncology. Biology. Physics
Volume: 77
Pages: 235-243
DOI
Peer Reviewed
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