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Fanconi anemia: at the Crossroads of DNA repair
Journal article   Peer reviewed

Fanconi anemia: at the Crossroads of DNA repair

J. S. Deakyne and A. V. Mazin
Biochemistry (Moscow), v 76(1), pp 36-48
01 Jan 2011
PMID: 21568838

Abstract

Biochemistry & Molecular Biology Life Sciences & Biomedicine Science & Technology
Fanconi anemia (FA) is an autosomal disorder that causes genome instability. FA patients suffer developmental abnormalities, early-onset bone marrow failure, and a predisposition to cancer. The disease is manifested by defects in DNA repair, hypersensitivity to DNA crosslinking agents, and a high degree of chromosomal aberrations. The FA pathway comprises 13 disease-causing genes involved in maintaining genomic stability. The fast pace of study of the novel DNA damage network has led to the constant discovery of new FA-like genes involved in the pathway that when mutated lead to similar disorders. A majority of the FA proteins act as signal transducers and scaffolding proteins to employ other pathways to repair DNA. This review discusses what is known about the FA proteins and other recently linked FA-like proteins. The goal is to clarify how the proteins work together to carry out interstrand crosslink repair and homologous recombination-mediated repair of damaged DNA.

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25 citations in Scopus

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#3 Good Health and Well-Being

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Collaboration types
Domestic collaboration
International collaboration
Web of Science research areas
Biochemistry & Molecular Biology
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