| Literature DB >> 20066559 |
Yinong Duan1, Xingxin He, Huiguang Yang, Yuhong Ji, Tao Tao, Jinling Chen, Ling Hu, Fupeng Zhang, Xiaohong Li, Huimin Wang, Aiguo Shen, Xiang Lu.
Abstract
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 bacteria. 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.Entities:
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Year: 2010 PMID： 20066559 DOI： 10.1007/s10753-009-9173-8
Source DB: PubMed Journal: Inflammation ISSN： 0360-3997 Impact factor: 4.092