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J. Biol. Chem., Vol. 279, Issue 6, 4713-4720, February 6, 2004

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Regulation of the Fanconi Anemia Group C Protein through Proteolytic Modification^*

Isabelle Brodeur, Isabelle Goulet, Cédric S. Tremblay, Chantal Charbonneau, Marie-Chantal Delisle, Chantal Godin, Caroline Huard, Edward W. Khandjian¶, Manuel Buchwald||**, Georges Lévesque¶, and Madeleine Carreau¶¶

From the Unité de Génétique Humaine et Moléculaire, CHUQ-Pavillon St-François d'Assise, Quebec, Quebec G1L 3L5, Canada, the Department of Pediatrics, Université Laval, Cité Universitaire, Quebec G1K 7P4, Canada, the ^¶Department of Medical Biology, Université Laval, Cité Universitaire, Quebec G1K 7P4, Canada, the ^||Program in Genetics and Genomic Biology, Research Institute, Hospital for Sick Children, Toronto, Ontario M5G 1X8, Canada, and the ^**Department of Molecular and Medical Genetics, University of Toronto, Toronto, Ontario M5G 1A8, Canada

The function of the Fanconi anemia group C protein (FANCC) is still unknown, though many studies point to a role in damage response signaling. Unlike other known FA proteins, FANCC is mainly localized to the cytoplasm and is thought to act as a messenger of cellular damage rather than an effector of repair. FANCC has been shown to interact with several cytoplasmic and nuclear proteins and to delay the onset of apoptosis through redox regulation of GSTP1. We investigated the fate and function of FANCC during apoptosis. Here we show that FANCC undergoes proteolytic modification by a caspase into a predominant 47-kDa ubiquitinated protein fragment. Lack of proteolytic modification at the putative cleavage site delays apoptosis but does not affect MMC complementation. These results suggest that FANCC function is regulated through proteolytic processing.

Received for publication, February 5, 2003 , and in revised form, October 22, 2003.

^* This work was supported by grants from the Fanconi Canada foundation (to M. C.), the Canadian Institutes of Health Research (CIHR; to M. C., M. B., and G. L.), the Fanconi Anemia Research Fund, Inc. (to M. C.), the Anemia Institute for Research and Education (to M. C.), the National Cancer Institute of Canada (NCIC) with funds from the Canadian Cancer Society (to M. B.), a CIHR junior investigator award (to M. C.), a FRSQ junior investigator award (to G. L.), and training awards from "La Fondation de la recherche sur les maladies infantiles (to I. G. and C. S. T.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

These authors contributed equally to this work.

Holds the Lombard Insurance Chair in Pediatric Research at the Hospital for Sick Children and the University of Toronto.

^¶¶ To whom correspondence should be addressed. Tel.: 418-525-4402; Fax: 418-525-4195; E-mail: Madeleine.Carreau{at}crsfa.ulaval.ca.

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