期刊
INFLAMMATION
卷 33, 期 3, 页码 189-199出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10753-009-9173-8
关键词
CDK11(p58); Cyclin D3; proliferation; apoptosis; Schwann cells; lipopolysaccharide
资金
- National Natural Science Foundation of China [30770488, 30870320]
- Natural Science Foundation of Jiangsu province [BK2006547]
- Health Project of Jiangsu Province [H200632]
- Financial Assistance of Jiangsu Province Grant
- Society and Technology Grew Project of Nantong City [S2008020]
Schwann cells proliferation is the main characterize of kinds PNS inflammation diseases. It has been well documented that cyclin D3 /CDK11(p58) complex inhibits cell function through multiple mechanisms, but the mechanism of cyclin D3/CDK11(p58) complex exerts its repressive role in the Schwann cells proliferation remains to be identified. In the present investigation, we demonstrated that the expression of CDK11(p58) were upregulated in the inflammation caused by LPS, a main part of bactria. Cyclin D3 and the 58-kDa isoform of cyclin-dependent kinase 11 (CDK11(p58)) interacted with each other mainly in nuclear region, repressed Schwann cells proliferation and induced cell apoptosis. Overexpression of CDK11(p58) expression might enhance this process, while silence of cyclin D3 reverting it. This work demonstrates for the first time the role of cyclin D3/CDK11(p58) complex in repressing the Schwann cells proliferation and inducing its apoptosis.
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