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Activation of c-Jun amino-terminal kinase by GDNF induces G2/M cell cycle delay linked with actin reorganization.
- Source :
- Genes to Cells; Jul2005, Vol. 10 Issue 7, p655-663, 9p
- Publication Year :
- 2005
-
Abstract
- It is well known that the cell cycle is controlled by several cyclin/cyclin-dependent kinase (Cdk) complexes whose expression and phosphorylation states vary with orderly periodicity. During the cell cycle, activity of the cyclin/Cdk complexes can be regulated directly or indirectly by a number of molecules, including protein kinases and phosphatases, p53, and Cdk inhibitors. Here, we show that the addition of glial cell line-derived neurotrophic factor (GDNF) induced G2/M cell cycle delay in human SK-N-MC neuroectodermal tumor cells that express RET tyrosine kinase, accompanying actin reorganization. Cell cycle delay at G2/M was characterized by accelerated and prolonged Cdc2 phosphorylation and stabilization of cyclin B1 and Wee1 kinase expression. Interestingly, we found that phosphorylation and/or expression of Cdc2, cyclinB1, and Wee1 was controlled by the Rac1/c-Jun NH<subscript>2</subscript>-terminal kinase (JNK) pathway. Immunohistochemical analysis suggested that the G2/M cell cycle delay may be necessary to prevent the mitotic progression of SK-N-MC cells with perturbed actin cytoskeletons. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 13569597
- Volume :
- 10
- Issue :
- 7
- Database :
- Complementary Index
- Journal :
- Genes to Cells
- Publication Type :
- Academic Journal
- Accession number :
- 17354796
- Full Text :
- https://doi.org/10.1111/j.1365-2443.2005.00866.x