title: 3R coordination by Fanconi anemia proteins.
abstract: Fanconi anemia (FA) is a recessive cancer prone syndrome featuring bone marrow failure and hypersensitivity to DNA crosslinks. Nine FA genes have been isolated so far. The biochemical function(s) of the FA proteins remain(s) poorly determined. However, a large consensus exists on the evidence that, to cope with DNA cross-links, a cell needs a functional FA pathway. In this review, we resume current understanding of how the FA pathway works in response to DNA damage and how it is integrated in a complex network of proteins involved in the maintenance of the genetic stability.
authors.affiliation: Institut Gustave-Roussy PR2, UPR2169 du CNRS, 39, rue Camille-Desmoulins, 94805 Villejuif cedex, France.
authors.forename: Gaëtane
authors.initials: G
authors.lastname: Macé
authors.forename: Massimo
authors.initials: M
authors.lastname: Bogliolo
authors.forename: Jean-Hugues
authors.initials: JH
authors.lastname: Guervilly
authors.forename: Jean Antoine
authors.initials: JA
authors.lastname: Dugas du Villard
authors.forename: Filippo
authors.initials: F
authors.lastname: Rosselli
mesh_terms: D002453:Cell Cycle; D018797:Cell Cycle Proteins / Q000378:metabolism*; D004249:DNA Damage; D004260:DNA Repair; D004261:DNA Replication; D004268:DNA-Binding Proteins / Q000378:metabolism*; D005199:Fanconi Anemia / Q000235:genetics* / Q000378:metabolism; D051856:Fanconi Anemia Complementation Group Proteins; D005786:Gene Expression Regulation; D030342:Genetic Diseases, Inborn / Q000235:genetics; D042822:Genomic Instability; D006801:Humans; D009687:Nuclear Proteins / Q000378:metabolism*; D013577:Syndrome
chemical_list: D018797:Cell Cycle Proteins; D004268:DNA-Binding Proteins; D051856:Fanconi Anemia Complementation Group Proteins; D009687:Nuclear Proteins