BRCA2 antagonizes classical and alternative nonhomologous end-joining to prevent gross genomic instability

Jinhua Han; Chunyan Ruan; Michael S. Y. Huen; Jiadong Wang; Anyong Xie; Chun Fu; Ting Liu; Jun Huang

doi:10.1038/s41467-017-01759-y

Nature Communications (Nov 2017)

BRCA2 antagonizes classical and alternative nonhomologous end-joining to prevent gross genomic instability

Jinhua Han,
Chunyan Ruan,
Michael S. Y. Huen,
Jiadong Wang,
Anyong Xie,
Chun Fu,
Ting Liu,
Jun Huang

Affiliations

Jinhua Han: Life Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University
Chunyan Ruan: Life Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University
Michael S. Y. Huen: School of Biomedical Sciences, Li Ka Shing Faculty of Medicine, The University of Hong Kong
Jiadong Wang: Institute of Systems Biomedicine, Department of Radiation Medicine, School of Basic Medical Sciences, Peking University Health Science Center
Anyong Xie: Institute of Translational Medicine, College of Medicine, Zhejiang University
Chun Fu: Department of Obstetrics and Gynecology, The Second Xiangya Hospital of Central South University
Ting Liu: Department of Cell Biology, Zhejiang University School of Medicine
Jun Huang: Life Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University

DOI: https://doi.org/10.1038/s41467-017-01759-y
Journal volume & issue: Vol. 8, no. 1
pp. 1 – 16

Abstract

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The genomic instability phenotype characteristic of BRCA2-deficient cells is not fully mechanistically understood. Here the authors show BRCA2 inactivation destabilizes RPA-coated single-stranded DNA and leads to toxic non homologous end-joining events.

Published in Nature Communications

ISSN: 2041-1723 (Online)
Publisher: Nature Portfolio
Country of publisher: United Kingdom
LCC subjects: Science
Website: https://www.nature.com/ncomms/

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