Parcs Is a Dual Regulator of Cell Proliferation and Apaf-1 Function
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CitationSanchez-Olea, Roberto, Sara Ortiz, Odmara Barreto, Qing Yang, Chi-jie Xu, Hong Zhu, and Junying Yuan. 2008. “Parcs Is a Dual Regulator of Cell Proliferation and Apaf-1 Function.” Journal of Biological Chemistry 283 (36): 24400–405. https://doi.org/10.1074/jbc.m804664200.
AbstractHere 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 G(1) 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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