BRD4 promotes resection and homology-directed repair of DNA double-strand breaks

John K. Barrows; Baicheng Lin; Colleen E. Quaas; George Fullbright; Elizabeth N. Wallace; David T. Long

doi:10.1038/s41467-022-30787-6

Nature Communications (May 2022)

BRD4 promotes resection and homology-directed repair of DNA double-strand breaks

John K. Barrows,
Baicheng Lin,
Colleen E. Quaas,
George Fullbright,
Elizabeth N. Wallace,
David T. Long

Affiliations

John K. Barrows: Department of Biochemistry and Molecular Biology, Medical University of South Carolina
Baicheng Lin: Department of Biochemistry and Molecular Biology, Medical University of South Carolina
Colleen E. Quaas: Department of Biochemistry and Molecular Biology, Medical University of South Carolina
George Fullbright: Department of Biochemistry and Molecular Biology, Medical University of South Carolina
Elizabeth N. Wallace: Department of Biochemistry and Molecular Biology, Medical University of South Carolina
David T. Long: Department of Biochemistry and Molecular Biology, Medical University of South Carolina

DOI: https://doi.org/10.1038/s41467-022-30787-6
Journal volume & issue: Vol. 13, no. 1
pp. 1 – 10

Abstract

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BRD4 is a multifunctional regulator of chromatin binding that plays a direct role in DNA double-strand break repair. BRD4 interacts with the SWI/SNF chromatin remodeling complex and resection machinery to promote homologous recombination.

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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