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Enforced expression of PPP1R13L increases tumorigenesis and invasion through p53-dependent and p53-independent mechanisms. Nature Precedings
Magdalena J. Laska; Scott Lowe; Lars Zender; Stephen Hearn; Ulla Vogel; Uffe Birk Jensen; Anka Bric; Bjørn A. Nexø.
PPP1R13L was initially identified as a protein that binds to the NF-[kappa]B subunit p65/RelA and inhibits its transcriptional activity. It also binds p53 and inhibits its action. One set of experimental findings based on over-expression of PPP1R13L indicates that PPP1R13L blocks apoptosis. Another set of experiments, based on endogenous production of PPP1R13L, suggests that the protein may sometimes be pro-apoptotic. We have used primary mouse embryonic fibroblasts (MEFs), dually transformed by H-ras and Adenovirus E1A and differing in their p53 status, to explore the effects of PPP1R13L over-expression, thus examining the ability of PPP1R13L to act as an oncoprotein. We found that over-expression of PPP1R13L strongly accelerated tumor formation by...
Tipo: Manuscript Palavras-chave: Cancer.
Ano: 2008 URL: http://precedings.nature.com/documents/2004/version/1
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