ATR kinase inhibition induces unscheduled origin firing through a Cdc7-dependent association between GINS and And-1

Tatiana Moiseeva; Brian Hood; Sandy Schamus; Mark J. O’Connor; Thomas P. Conrads; Christopher J. Bakkenist

doi:10.1038/s41467-017-01401-x

Nature Communications (Nov 2017)

ATR kinase inhibition induces unscheduled origin firing through a Cdc7-dependent association between GINS and And-1

Tatiana Moiseeva,
Brian Hood,
Sandy Schamus,
Mark J. O’Connor,
Thomas P. Conrads,
Christopher J. Bakkenist

Affiliations

Tatiana Moiseeva: Department of Radiation Oncology, University of Pittsburgh School of Medicine, Hillman Cancer Center
Brian Hood: Inova Schar Cancer Institute, Inova Center for Personalized Health
Sandy Schamus: Department of Radiation Oncology, University of Pittsburgh School of Medicine, Hillman Cancer Center
Mark J. O’Connor: DNA Damage Response Biology, Innovative Medicines and Early Clinical Development
Thomas P. Conrads: Inova Schar Cancer Institute, Inova Center for Personalized Health
Christopher J. Bakkenist: Department of Radiation Oncology, University of Pittsburgh School of Medicine, Hillman Cancer Center

DOI: https://doi.org/10.1038/s41467-017-01401-x
Journal volume & issue: Vol. 8, no. 1
pp. 1 – 11

Abstract

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ATR kinase activity is essential for slowing replication forks and preventing DNA replication in cells with DNA damage. Here the authors show that ATR inhibition leads to Cdc7 phosphorylation of GINS, leading to origin firing.

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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