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The Multiple Battles Fought by Anti-Apoptotic p21
Reiner U. Jänicke, Dennis Sohn, Frank Essmann and Klaus Schulze-Osthoff
volume 6 | issue 4
15 February 2007Pages: 407 - 413
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Until recently, the p53 transcriptional target p21, a member of the Cip/Kip family, was almost solely viewed as a nuclear protein with a principal function of inhibiting cyclin-dependent kinase (CDK) activity and hence, cell cycle progression. However, emerging evidence now suggests additional functions for p21 in diverse cellular processes including a role as a modulator of apoptosis. Several mechanisms are suggested by which p21 interferes with the apoptotic machinery that encompass either CDK-independent events such as transcriptional regulation and direct binding to pro-apoptotic gene products in the cytoplasm, or that were based on inhibition of CDKs that in several studies were required downstream of caspases for the generation of characteristic apoptotic alterations. Very recently, we have shown that p21 protects cells from irradiation-induced apoptosis by suppression of CDK activity that appears to be required downstream of the mitochondria for an efficient activation of the caspase cascade. Together with other reports, our results not only demonstrate the close connection of events leading to either cell cycle arrest or apoptosis, but also indicate that the CDK inhibitor p21 battles apoptosis at multiple frontiers.
Authors
Reiner U. Jänicke
University of Düsseldorf, Institute of Molecular Medicine; Düsseldorf, Germany
Dennis Sohn
University of Düsseldorf, Institute of Molecular Medicine; Düsseldorf, Germany
Frank Essmann
University of Düsseldorf, Institute of Molecular Medicine; Düsseldorf, Germany
Klaus Schulze-Osthoff
University of Düsseldorf, Institute of Molecular Medicine; Düsseldorf, Germany
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.




