Abstract:
:Fanconi anemia (FA) is an autosomal or X-linked recessive disorder characterized by chromosomal instability, bone marrow failure, cancer susceptibility, and a profound sensitivity to agents that produce DNA interstrand cross-link (ICL). To date, 15 genes have been identified that, when mutated, result in FA or an FA-like syndrome. It is believed that cellular resistance to DNA interstrand cross-linking agents requires all 15 FA or FA-like proteins. Here, we review our current understanding of how these FA proteins participate in ICL repair and discuss the molecular mechanisms that regulate the FA pathway to maintain genome stability.
journal_name
Protein Celljournal_title
Protein & cellauthors
Su X,Huang Jdoi
10.1007/s13238-011-1098-ysubject
Has Abstractpub_date
2011-09-01 00:00:00pages
704-11issue
9eissn
1674-800Xissn
1674-8018journal_volume
2pub_type
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