New roads to FA/BRCA pathway: H2AX

Alex Lyakhovich; Jordi Surrallés

doi:10.4161/cc.6.9.4223

New roads to FA/BRCA pathway: H2AX

Alex Lyakhovich, Jordi Surrallés

Department of Genetics and Microbiology

Research output: Contribution to journal › Review article › Research › peer-review

18 Citations (Scopus)

Abstract

We have recently described an involvement of H2AX into the Fanconi anemia (FA) BRCA pathway through recruitment of FA protein FANCD2 to the sites of stalled replication forks. We showed that BRCA1 mediates the recruitment of FANCD2 by γH2AX to damaged chromatin and cells deficient or depleted of H2AX exhibit an FA-like phenotype, including an excess of chromatid-type chromosomal aberrations and hypersensitivity to MMC. Here, we discuss a model for the FA pathway and how it could partially explain the common phenotypes of H2AX, BRCA2 and FA deficiencies. ©2007 Landes Bioscience.

Original language	English
Pages (from-to)	1019-1023
Journal	Cell Cycle
Volume	6
Issue number	9
DOIs	https://doi.org/10.4161/cc.6.9.4223
Publication status	Published - 1 May 2007

Keywords

BRCA2
DNA repair
FANCD2
Fanconi anemia
Histone H2AX
Stalled replication fork

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title = "New roads to FA/BRCA pathway: H2AX",

abstract = "We have recently described an involvement of H2AX into the Fanconi anemia (FA) BRCA pathway through recruitment of FA protein FANCD2 to the sites of stalled replication forks. We showed that BRCA1 mediates the recruitment of FANCD2 by γH2AX to damaged chromatin and cells deficient or depleted of H2AX exhibit an FA-like phenotype, including an excess of chromatid-type chromosomal aberrations and hypersensitivity to MMC. Here, we discuss a model for the FA pathway and how it could partially explain the common phenotypes of H2AX, BRCA2 and FA deficiencies. {\textcopyright}2007 Landes Bioscience.",

keywords = "BRCA2, DNA repair, FANCD2, Fanconi anemia, Histone H2AX, Stalled replication fork",

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T1 - New roads to FA/BRCA pathway: H2AX

AU - Lyakhovich, Alex

AU - Surrallés, Jordi

PY - 2007/5/1

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N2 - We have recently described an involvement of H2AX into the Fanconi anemia (FA) BRCA pathway through recruitment of FA protein FANCD2 to the sites of stalled replication forks. We showed that BRCA1 mediates the recruitment of FANCD2 by γH2AX to damaged chromatin and cells deficient or depleted of H2AX exhibit an FA-like phenotype, including an excess of chromatid-type chromosomal aberrations and hypersensitivity to MMC. Here, we discuss a model for the FA pathway and how it could partially explain the common phenotypes of H2AX, BRCA2 and FA deficiencies. ©2007 Landes Bioscience.

AB - We have recently described an involvement of H2AX into the Fanconi anemia (FA) BRCA pathway through recruitment of FA protein FANCD2 to the sites of stalled replication forks. We showed that BRCA1 mediates the recruitment of FANCD2 by γH2AX to damaged chromatin and cells deficient or depleted of H2AX exhibit an FA-like phenotype, including an excess of chromatid-type chromosomal aberrations and hypersensitivity to MMC. Here, we discuss a model for the FA pathway and how it could partially explain the common phenotypes of H2AX, BRCA2 and FA deficiencies. ©2007 Landes Bioscience.

KW - BRCA2

KW - DNA repair

KW - FANCD2

KW - Fanconi anemia

KW - Histone H2AX

KW - Stalled replication fork

U2 - 10.4161/cc.6.9.4223

DO - 10.4161/cc.6.9.4223

M3 - Review article

VL - 6

SP - 1019

EP - 1023

IS - 9

ER -

New roads to FA/BRCA pathway: H2AX

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Keywords

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