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Cell Cycling through Cdc25A: Transducer of Cytokine Proliferative Signals
C. Kittipatarin, WQ. Li, D. Bulavin, S.K. Durum and A.R. Khaled
volume 5 | issue 9
1 may 2006Pages: 907 - 912
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A balance between survival and proliferative signals maintains a constant number of T lymphocytes that populate the mammalian immune system, a process termed “homeostasis”. Central to this process is the availability of a stromal cell product – the cytokine interleukin-7 (IL-7). We recently showed that IL-7, in addition to protecting cells from apoptosis, drives the cell cycling of lymphocytes through regulation of the stability of the phosphatase, Cdc25A, a key activator of cyclin-dependent kinases (cdks). IL-7 achieves this by controlling the activity of p38 MAP kinase (MAPK), which can phosphorylate Cdc25A, triggering its degradation. Sustained expression of Cdc25A had diverse effects: it promoted cell cycling, even in presence of cell cycle inhibitors such p27Kip1, and prevented cell shrinkage in response to cytokine deprivation. Herein we show a role for Cdc25A as a transducer of cytokine-driven proliferation and discuss novel implications for cell growth from the perspective of the requirements for maintenance of lymphocyte homeostasis.
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.