Journal
CELL CYCLE
Volume 4, Issue 1, Pages 57-62Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.4.1.1357
Keywords
topoisomerase II; p38; antephase; stress reponse; checkpoint; mitosis
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Funding
- NIGMS NIH HHS [GMS 40198] Funding Source: Medline
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM040198, R37GM040198] Funding Source: NIH RePORTER
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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 G(2) 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, down-regulates 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.
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