Identification and characterization of p53-target genes
Project/Area Number |
17013089
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Research Category |
Grant-in-Aid for Scientific Research on Priority Areas
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Allocation Type | Single-year Grants |
Review Section |
Biological Sciences
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Research Institution | National Cancer Center Research Institute and Research Center for Innovative Oncology, National Cancer Center Hospital East |
Principal Investigator |
ARAKAWA Hirofumi National Cancer Center Research Institute and Research Center for Innovative Oncology, National Cancer Center Hospital East, 生物物理部, 部長 (70313088)
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Project Period (FY) |
2005 – 2009
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Project Status |
Completed (Fiscal Year 2009)
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Budget Amount *help |
¥41,800,000 (Direct Cost: ¥41,800,000)
Fiscal Year 2009: ¥8,300,000 (Direct Cost: ¥8,300,000)
Fiscal Year 2008: ¥8,300,000 (Direct Cost: ¥8,300,000)
Fiscal Year 2007: ¥8,300,000 (Direct Cost: ¥8,300,000)
Fiscal Year 2006: ¥8,300,000 (Direct Cost: ¥8,300,000)
Fiscal Year 2005: ¥8,600,000 (Direct Cost: ¥8,600,000)
|
Keywords | p53 / 転写 / 標的遺伝子 / がん / マイクロアレイ / がん抑制遺伝子 / ミトコンドリア / 品質管理 / 細胞質分裂 / 染色体異数性 / オートファジー / がん治療 / 細胞死 / DNA損傷 / 血管新生 / 腫瘍血管 |
Research Abstract |
In the present study, we identified and characterized seven novel p53-target genes ; DFNA5, SEMA3F, BLNK, UNC5A, TMPS, NEEP21 and Mieap. DFNA5, UNC5A, TMPS and NEEP21 are involved in p53-dependent apoptosis. SEMA3F is a mediator of p53-regulated anti-angiogenesis. Discovery of these genes could provide more information to two major functions of p53 ; cell death and anti-angiogenesis. On the other hand, discovery of BLNK and Mieap demonstrates that there are very novel pathways for p53 tumor suppression. BLNK prevents aneuploidy by inhibiting cytokinesis after DNA damage, leading to maintenance of genomic stability. Moreover, Mieap plays an essential role in mitochondrial quality control. These findings could not only shed light on the mechanism of p53 tumor suppression but also contribute to understanding of cancer nature.
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Report
(6 results)
Research Products
(42 results)
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[Journal Article] Mutation of RRM2B, encoding p53-controlled ribonucleotide reductase (p53R2), causes severe mitochondrial DNA depletion.2007
Author(s)
Bourdon A, Minai L, Serre V, Jais JP, Sarzi E, Aubert S, Chretien D, de Lonlay P, Paquis-Flucklinger V, Arakawa H, Nakamura Y, Munnich A, Rotig A.
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Journal Title
Nat Genet 39
Pages: 776-780
Related Report
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[Journal Article] The potential role of DFNA5, a hearing impairment gene, in p53-mediated cellular response to DNA damage.2006
Author(s)
Masuda Y, Futamura M, Kamino H, Nakamura Y, Kitamura N, Ohnishi S, Miyamoto Y, Ichikawa H, Ohta T, Ohki M, Kiyono T, Egami H, Baba H, Arakawa H.
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Journal Title
J Hum Genet 51
Pages: 652-664
NAID
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[Journal Article] Identification of NEEP21, encoding neuron-enriched endosomal protein of 21 kDa, as a transcriptional target of tumor suppressor p53.
Author(s)
Ohnishi S, Futamura M, Kamino H, Nakamura Y, Kitamura N, Miyamoto Y, Miyamoto T, Shinogi D, Goda O, Arakawa H.
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Journal Title
Related Report
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