A role for the Fanconi anemia C protein in maintaining the DNA damage-induced G2 checkpoint

The Journal of Biological Chemistry
Brian FreieD Wade Clapp

Abstract

Fanconi anemia (FA) is a complex, heterogeneous genetic disorder composed of at least 11 complementation groups. The FA proteins have recently been found to functionally interact with the cell cycle regulatory proteins ATM and BRCA1; however, the function of the FA proteins in cell cycle control remains incompletely understood. Here we show that the Fanconi anemia complementation group C protein (Fancc) is necessary for proper function of the DNA damage-induced G2/M checkpoint in vitro and in vivo. Despite apparently normal induction of the G2/M checkpoint after ionizing radiation, murine and human cells lacking functional FANCC did not maintain the G2 checkpoint as compared with wild-type cells. The increased rate of mitotic entry seen in Fancc-/-mouse embryo fibroblasts correlated with decreased inhibitory phosphorylation of cdc2 kinase on tyrosine 15. An increased inability to maintain the DNA damage-induced G2 checkpoint was observed in Fancc -/-; Trp53 -/-cells compared with Fancc -/-cells, indicating that Fancc and p53 cooperated to maintain the G2 checkpoint. In contrast, genetic disruption of both Fancc and Atm did not cooperate in the G2 checkpoint. These data indicate that Fancc and p53 in separate pathways converge t...Continue Reading

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Citations

Jul 28, 2009·The Journal of Biological Chemistry·Alexandra SobeckMaureen E Hoatlin
Jul 17, 2008·Antioxidants & Redox Signaling·Wei DuQishen Pang
Dec 1, 2011·Nucleic Acids Research·Hiroshi ArakawaGeorge Iliakis
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May 23, 2018·Stem Cell Research & Therapy·Wei DuQishen Pang
Dec 17, 2005·Genes & Development·Richard D Kennedy, Alan D D'Andrea

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