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Publication : Parcs is a dual regulator of cell proliferation and apaf-1 function.

First Author  Sanchez-Olea R Year  2008
Journal  J Biol Chem Volume  283
Issue  36 Pages  24400-5
PubMed ID  18562310 Mgi Jnum  J:141771
Mgi Id  MGI:3819721 Doi  10.1074/jbc.M804664200
Citation  Sanchez-Olea R, et al. (2008) Parcs is a dual regulator of cell proliferation and apaf-1 function. J Biol Chem 283(36):24400-5
abstractText  Here we identify a novel protein, named Parcs for pro-apoptotic protein required for cell survival, that is involved in both cell cycle progression and apoptosis. Parcs interacted with Apaf-1 by binding to the oligomerization domain of Apaf-1. Apaf-1-mediated activation of caspase-9 and caspase-3 was markedly decreased in a cytosolic fraction isolated from HeLa cells with reduced parcs expression. Interestingly, parcs deficiency blocked cell proliferation in non-tumorigenic cells but not in multiple tumor cell lines. In MCF-10A cells, parcs deficiency led to early G1 arrest. Conditional inactivation of parcs in genetically modified primary mouse embryonic fibroblasts using the Cre-LoxP system also resulted in the inhibition of cell proliferation. We conclude that Parcs may define a molecular checkpoint in the control of cell proliferation for normal cells that is lost in tumor cells.
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