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. |