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Expanded roles of the Fanconi anemia pathway in preserving genomic stability Kee Y; D'Andrea ADGenes Dev 2010[Aug]; 24 (16): 1680-94Studying rare human genetic diseases often leads to a better understanding of normal cellular functions. Fanconi anemia (FA), for example, has elucidated a novel DNA repair mechanism required for maintaining genomic stability and preventing cancer. The FA pathway, an essential tumor-suppressive pathway, is required for protecting the human genome from a specific type of DNA damage; namely, DNA interstrand cross-links (ICLs). In this review, we discuss the recent progress in the study of the FA pathway, such as the identification of new FANCM-binding partners and the identification of RAD51C and FAN1 (Fanconi-associated nuclease 1) as new FA pathway-related proteins. We also focus on the role of the FA pathway as a potential regulator of DNA repair choices in response to double-strand breaks, and its novel functions during the mitotic phase of the cell cycle.|Animals[MESH]|DNA Damage/genetics[MESH]|DNA Repair/genetics[MESH]|DNA-Binding Proteins/genetics/metabolism[MESH]|Endodeoxyribonucleases[MESH]|Exodeoxyribonucleases/metabolism[MESH]|Fanconi Anemia/*genetics/*physiopathology[MESH]|Genomic Instability/*genetics[MESH]|Humans[MESH]|Multifunctional Enzymes[MESH]|Mutation[MESH]|Protein Binding[MESH]|Tumor Suppressor Proteins/metabolism[MESH] |
