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A Novel Role of p38α MAPK in Mitotic Progression Independent of Its Kinase Activity
Li Fan, Xianlin Yang, Jian Du, Mark Marshall, Kerry Blanchard and Xiang Ye
volume 4 | issue 11
November 2005Pages: 1616 - 1624
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Activation of p38α MAPK triggers G2/M checkpoint, thus inhibiting cell proliferation. In this study we found that depletion of p38α by RNAi also inhibited cell proliferation and caused mitotic arrest. However, treatment with selective small molecule p38 kinase inhibitors had no effect on cell cycle progression, even though the p38 kinase was completely inhibited, revealing p38α functions that are independent of its kinase activity. Indeed, ectopic expression of a kinase negative p38α rescued the lethality caused by RNAi-depletion of the endogenous p38α, thus providing further evidence for a kinase-independent function of p38α. In addition, we showed that overexpression of the wild type or kinase-negative p38α also strongly inhibited cell proliferation, similarly as RNAi depletion of p38α. Together the results demonstrate that, in addition to its kinase-dependent functions, such as in activation of G2/M checkpoint, p38α also has an essential, kinase-independent function.
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF 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.