A protective role for BRCA2 at stalled replication forks

The hereditary breast and ovarian cancer predisposition genes BRCA1 and BRCA2 account for the lion's share of heritable breast cancer risk in the human population. Loss of function of either gene results in defective homologous recombination (HR) and triggers genomic instability, accelerating b...

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Detalles Bibliográficos
Autores principales: Chandramouly, Gurushankar, Willis, Nicholas A, Scully, Ralph
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2011
Materias:
Viewpoint
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3262192/
https://www.ncbi.nlm.nih.gov/pubmed/21996371
http://dx.doi.org/10.1186/bcr2918
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author Chandramouly, Gurushankar
Willis, Nicholas A
Scully, Ralph
author_facet Chandramouly, Gurushankar
Willis, Nicholas A
Scully, Ralph
author_sort Chandramouly, Gurushankar
collection PubMed
description The hereditary breast and ovarian cancer predisposition genes BRCA1 and BRCA2 account for the lion's share of heritable breast cancer risk in the human population. Loss of function of either gene results in defective homologous recombination (HR) and triggers genomic instability, accelerating breast tumorigenesis. A long-standing hypothesis proposes that BRCA1 and BRCA2 mediate HR following attempted replication across damaged DNA, ensuring error-free processing of the stalled replication fork. A recent paper describes a new replication fork protective function of BRCA2, which appears to collaborate with its HR function to suppress genomic instability.
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spelling pubmed-32621922012-03-07 A protective role for BRCA2 at stalled replication forks Chandramouly, Gurushankar Willis, Nicholas A Scully, Ralph Breast Cancer Res Viewpoint The hereditary breast and ovarian cancer predisposition genes BRCA1 and BRCA2 account for the lion's share of heritable breast cancer risk in the human population. Loss of function of either gene results in defective homologous recombination (HR) and triggers genomic instability, accelerating breast tumorigenesis. A long-standing hypothesis proposes that BRCA1 and BRCA2 mediate HR following attempted replication across damaged DNA, ensuring error-free processing of the stalled replication fork. A recent paper describes a new replication fork protective function of BRCA2, which appears to collaborate with its HR function to suppress genomic instability. BioMed Central 2011 2011-09-07 /pmc/articles/PMC3262192/ /pubmed/21996371 http://dx.doi.org/10.1186/bcr2918 Text en Copyright ©2010 BioMed Central Ltd
spellingShingle Viewpoint
Chandramouly, Gurushankar
Willis, Nicholas A
Scully, Ralph
A protective role for BRCA2 at stalled replication forks
title A protective role for BRCA2 at stalled replication forks
title_full A protective role for BRCA2 at stalled replication forks
title_fullStr A protective role for BRCA2 at stalled replication forks
title_full_unstemmed A protective role for BRCA2 at stalled replication forks
title_short A protective role for BRCA2 at stalled replication forks
title_sort protective role for brca2 at stalled replication forks
topic Viewpoint
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3262192/
https://www.ncbi.nlm.nih.gov/pubmed/21996371
http://dx.doi.org/10.1186/bcr2918
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