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Perspectives
The p38-Mediated Stress-Activated Checkpoint: A Rapid Response System for Delaying Progression through Antephase and Entry into Mitosis
Alexei Mikhailov, Mio Shinohara and Conly L. Rieder
volume 4 | issue 1
january 2005Pages: 57 - 62
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Cells have evolved a number of control pathways that delay or prevent them from entering mitosis under conditions that can compromise genome integrity. One recently appreciated and versatile control pathway involves the p38 stress activated protein kinase. During late G2 p38 is rapidly activated by diverse stresses (topoisomerase II (topo II)) and histone deacetylase inhibitors, osmotic shock, microtubule disassembly, UV light, etc) via a number of different pathways. Once activated p38 appears to delay entry into mitosis by inhibiting cdc25B phosphatase that, in turn, downregulates cyclin A/CDK2 activity. Depending on the agent and degree of stress, this delay may be transient, or it may last until transcription mediated checkpoint pathways can take over.
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.




