Conference Proceedings

FANCD2 monoubiquitination and activation by hexavalent chromium [Cr(VI)] exposure: Activation is not required for repair of Cr(VI)-induced DSBS

Susan K Vilcheck, Susan Ceryak, Travis J O'Brien, Steven R Patierno

Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis | ELSEVIER SCIENCE BV | Published : 2006

Abstract

Fanconi anemia (FA) is a rare autosomal recessive disorder characterized by congenital abnormalities, progressive bone marrow failure, and cancer susceptibility. FA cells are hypersensitive to DNA crosslinking agents. FA is a genetically heterogeneous disease with at least 11 complementation groups. The eight cloned FA proteins interact in a common pathway with established DNA-damage-response proteins, including BRCA1 and ATM. Six FA proteins (A, C, E, F, G, and L) regulate the monoubiquitination of FANCD2 after DNA damage by crosslinking agents, which targets FANCD2 to BRCA1 nuclear foci containing BRCA2 (FANCD1) and RAD51. Some forms of hexavalent chromium [Cr(VI)] are implicated as respir..

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