Role of CDK inhibitors in self-renewal regulation of spermatogonial stem cell
Project/Area Number |
26293064
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Partial Multi-year Fund |
Section | 一般 |
Research Field |
General medical chemistry
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Research Institution | Kyoto University |
Principal Investigator |
Shinohara Mito 京都大学, 医学(系)研究科(研究院), 助教 (10372591)
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Project Period (FY) |
2014-04-01 – 2017-03-31
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Project Status |
Completed (Fiscal Year 2016)
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Budget Amount *help |
¥15,990,000 (Direct Cost: ¥12,300,000、Indirect Cost: ¥3,690,000)
Fiscal Year 2016: ¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2014: ¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
|
Keywords | 幹細胞 / 細胞周期 / 生殖 / 自己複製 |
Outline of Final Research Achievements |
In this project, we investigated the involvement of p57 gene, one of the Cyclin-dependent kinase inhibitors (CDKIs), in the regulation of self-renewal and maintenance of spermatogonial stem cells (SSCs). The results showed that the expression of p57 gene was upregulated in SSCs by FGF2 and GDNF, the self-renewal factors of SSCs. Using cultured SSC cell lines, which were derived from conditional knockout mice of p57 gene, we identified that self-renewal activity of SSCs was reduced in vitro by p57 gene deficiency. To elucidate the signaling pathway, which mediates the effect of p57 gene, we screened for molecules by microarray analysis, whose expression levels were affected by p57 gene deficiency. Involvements of some of these molecules were confirmed by overexpression or knockdown in cultured SSC cell line.
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Report
(4 results)
Research Products
(26 results)
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[Journal Article] Pluripotent cell derivation from male germline cells by suppression of <i>Dmrt1</i> and <i>Trp53</i>2015
Author(s)
Tanaka, T., Kanatsu-Shinohara, M., Hirose, M., Ogura, A., Shinohara, T.
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Journal Title
Journal of Reproduction and Development
Volume: 61
Issue: 5
Pages: 473-484
DOI
NAID
ISSN
0916-8818, 1348-4400
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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