PAXX promotes KU accumulation at DNA breaks and is essential for end-joining in XLF-deficient mice

Xiangyu Liu; Zhengping Shao; Wenxia Jiang; Brian J. Lee; Shan Zha

doi:10.1038/ncomms13816

Nature Communications (Jan 2017)

PAXX promotes KU accumulation at DNA breaks and is essential for end-joining in XLF-deficient mice

Xiangyu Liu,
Zhengping Shao,
Wenxia Jiang,
Brian J. Lee,
Shan Zha

Affiliations

Xiangyu Liu: Department of Pathology and Cell Biology, College of Physicians and Surgeons, Institute for Cancer Genetics, Columbia University
Zhengping Shao: Department of Pathology and Cell Biology, College of Physicians and Surgeons, Institute for Cancer Genetics, Columbia University
Wenxia Jiang: Department of Pathology and Cell Biology, College of Physicians and Surgeons, Institute for Cancer Genetics, Columbia University
Brian J. Lee: Department of Pathology and Cell Biology, College of Physicians and Surgeons, Institute for Cancer Genetics, Columbia University
Shan Zha: Department of Pathology and Cell Biology, College of Physicians and Surgeons, Institute for Cancer Genetics, Columbia University

DOI: https://doi.org/10.1038/ncomms13816
Journal volume & issue: Vol. 8, no. 1
pp. 1 – 13

Abstract

Read online

Non-homologous end-joining is the key pathway for repairing double-stranded DNA breaks in mammalian cells. Here the authors show that PAXX promotes the accumulation of KU at DNA breaks and is essential for end-joining in cells lacking XLF.

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/

About the journal