Kinase-dead ATR differs from ATR loss by limiting the dynamic exchange of ATR and RPA

Demis Menolfi; Wenxia Jiang; Brian J. Lee; Tatiana Moiseeva; Zhengping Shao; Verna Estes; Mark G. Frattini; Christopher J. Bakkenist; Shan Zha

doi:10.1038/s41467-018-07798-3

Nature Communications (Dec 2018)

Kinase-dead ATR differs from ATR loss by limiting the dynamic exchange of ATR and RPA

Demis Menolfi,
Wenxia Jiang,
Brian J. Lee,
Tatiana Moiseeva,
Zhengping Shao,
Verna Estes,
Mark G. Frattini,
Christopher J. Bakkenist,
Shan Zha

Affiliations

Demis Menolfi: Institute for Cancer Genetics, Department of Pathology and Cell Biology, College of Physicians & Surgeons, Columbia University
Wenxia Jiang: Institute for Cancer Genetics, Department of Pathology and Cell Biology, College of Physicians & Surgeons, Columbia University
Brian J. Lee: Institute for Cancer Genetics, Department of Pathology and Cell Biology, College of Physicians & Surgeons, Columbia University
Tatiana Moiseeva: Department of Radiation Oncology, University of Pittsburgh School of Medicine, Hillman Cancer Center
Zhengping Shao: Institute for Cancer Genetics, Department of Pathology and Cell Biology, College of Physicians & Surgeons, Columbia University
Verna Estes: Institute for Cancer Genetics, Department of Pathology and Cell Biology, College of Physicians & Surgeons, Columbia University
Mark G. Frattini: Department of Medicine, College of Physicians & Surgeons, Columbia University
Christopher J. Bakkenist: Department of Radiation Oncology, University of Pittsburgh School of Medicine, Hillman Cancer Center
Shan Zha: Institute for Cancer Genetics, Department of Pathology and Cell Biology, College of Physicians & Surgeons, Columbia University

DOI: https://doi.org/10.1038/s41467-018-07798-3
Journal volume & issue: Vol. 9, no. 1
pp. 1 – 16

Abstract

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ATR kinase is a key regulator of chromosome integrity. Here the authors by analysing the phenotype of a mouse model expressing a kinase-dead ATR, reveal the effect of ATR inhibition compared to ATR loss and its consequences for meiosis, DNA replication, checkpoint activation and genome instability .

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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