期刊
GENES & DEVELOPMENT
卷 24, 期 16, 页码 1680-1694出版社
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.1955310
关键词
Fanconi anemia; DNA repair; interstrand cross-link (ICL); homologous recombination (HR); nonhomologous end-joining (NHEJ); mitosis
资金
- Leukemia and Lymphoma Society
- [R01DK43389]
- [R01HL52725]
Studying 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.
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