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- W2014623218 endingPage "1069" @default.
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- W2014623218 abstract "Fanconi anemia (FA) is a rare autosomal recessive disease characterized by chromosome instability and cancer predisposition. At least 11 complementation groups for FA have been identified, and eight FA genes have been cloned. Interestingly, the eight known FA proteins cooperate in a common pathway leading to the interaction of monoubiquitinated FANCD2 and BRCA2 in damaged chromatin. Disruption of this pathway results in the clinical and cellular abnormalities common to all FA subtypes. This review will examine the interaction of the cloned FA proteins with each other and with other DNA damage response proteins (i.e., ATM, ATR, and NBS1). Also, somatic (acquired) disruption of the FA pathway in human tumors appears to account for their chromosome instability and crosslinker hypersensitivity." @default.
- W2014623218 created "2016-06-24" @default.
- W2014623218 creator A5044648110 @default.
- W2014623218 creator A5076614946 @default.
- W2014623218 date "2004-08-01" @default.
- W2014623218 modified "2023-10-17" @default.
- W2014623218 title "The interplay of Fanconi anemia proteins in the DNA damage response" @default.
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- W2014623218 doi "https://doi.org/10.1016/j.dnarep.2004.04.005" @default.
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