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Role of the calpain-calpastatin system in the density-dependent growth arrest.

Authors: Stifanese, R  Averna, M  De Tullio, R  Salamino, F  Cantoni, C  Mingari, MC  Prato, C  Pontremoli, S  Melloni, E 
Citation: Stifanese R, etal., Arch Biochem Biophys. 2008 Nov 15;479(2):145-52. Epub 2008 Sep 13.
Pubmed: (View Article at PubMed) PMID:18809371
DOI: Full-text: DOI:10.1016/

In dividing cells calpastatin diffuses from aggregates into cytosol, indicating the requirement for a tight regulation of calpain. Accordingly, the involvement of the calpain-calpastatin system in cell proliferation and in the density-dependent growth arrest was studied in JA3 cells stably transfected with a calpastatin form permanently localized in cytosol. In calpastatin overexpressing cells, cell cycle rate is 50% reduced, and cells enter the ungrowing, still fully reversible, stage at a 3-fold higher cell density. Furthermore, in cell density growth arrest phase, down regulation of alpha- and theta-PKC isoforms, as well as FAK and talin occurs. In calpastatin overexpressing cells, degradation of these calpain substrate proteins is prevented and delayed. Thus, calpain activity plays a crucial role in inducing the cell entry into a functional quiescent phase.


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RGD Object Information
RGD ID: 5683637
Created: 2011-11-29
Species: All species
Last Modified: 2011-11-29
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.