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PMID: 15935541 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Review

3R coordination by Fanconi anemia proteins.

Biochimie ·Vol. 87 ·No. 7 ·2005-07-00 ·Pages 647-58

Macé G, Bogliolo M, Guervilly JH, Dugas du Villard JA, Rosselli F

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.

MeSH Terms
Cell Cycle Cell Cycle Proteins/metabolism DNA Damage DNA Repair DNA Replication DNA-Binding Proteins/metabolism Fanconi Anemia/genetics,metabolism Fanconi Anemia Complementation Group Proteins Gene Expression Regulation Genetic Diseases, Inborn/genetics Genomic Instability Humans Nuclear Proteins/metabolism Syndrome
Chemicals
Cell Cycle Proteins DNA-Binding Proteins Fanconi Anemia Complementation Group Proteins Nuclear Proteins
Authors & Affiliations
5 authors, click to expand affiliations / ORCID
Macé Gaëtane
Institut Gustave-Roussy PR2, UPR2169 du CNRS, 39, rue Camille-Desmoulins, 94805 Villejuif cedex, France.
Bogliolo Massimo
Guervilly Jean-Hugues
Dugas du Villard Jean Antoine
Rosselli Filippo
Article Info
Journal
Biochimie
Abbr.
Biochimie
ISSN
0300-9084
Published
2005-07-00
Pages
647-58
Language
English
Region
France
NLM ID
1264604
Subset
IM
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