2010 Fiscal Year Final Research Report
Study of the mammalian G1 regulatory mechanism unifying Rb and p53 pathways.
| Project/Area Number |
19370087
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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 |
Cell biology
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| Research Institution | Nara Institute of Science and Technology |
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Principal Investigator |
KATO Junya 奈良先端科学技術大学院大学, バイオサイエンス研究科, 教授 (00273839)
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| Co-Investigator(Kenkyū-buntansha) |
KATO Noriko 奈良先端科学技術大学院大学, バイオサイエンス研究科, 助教 (10252785)
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| Project Period (FY) |
2007 – 2010
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| Keywords | 遺伝学 / 癌 / シグナル伝達 / 細胞周期 / 哺乳類 |
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| Research Abstract |
We studied the regulatory mechanism of G1 progression of the mammalian cell cycle by focusing on how the COP9 signalosome complex regulates Rb and p53 pathways. We found that the fifth subunit of the COP9 signalosome(CSN5), through interaction with a histone methyltransferase, SMYD3, bound to the promoter region of the p16 gene and regulated its transcription, indicating that the signaling pathway consisting of CSN5, SMYD3, p16, cyclin D-Cdk4/6, and Rb plays an important role in regulation of the hematopoietic somatic stem cells. We also found that the third component, CSN3, participated in the regulation of the COP1-p53 pathway through MLF1.
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[Journal Article] Overexpression of adenovirus-mediated p27kip1 lacking the Jab1-binding region enhances cytotoxicity and inhibits xenografted human cholangiocarcinoma growth2009
Author(s)
Shiraso S, Katayose Y, Yamamoto K, Mizuma M, Yabuuchi S, Oda A, Rikiyama T, Onogawa T, Yoshida H, Hayashi H, Ohtsuka H, Motoi F, Egawa S, Kato J, Unno M.
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Journal Title
Anticancer Res
Volume: 29
Pages: 2015-24
Peer Reviewed
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