ATM orchestrates the DNA-damage response to counter toxic non-homologous end-joining at broken replication forks

Volume: 10, Issue: 1, Pages: 87 - 87
Published: Jan 8, 2019
Abstract
Mutations in the ATM tumor suppressor gene confer hypersensitivity to DNA-damaging chemotherapeutic agents. To explore genetic resistance mechanisms, we performed genome-wide CRISPR-Cas9 screens in cells treated with the DNA topoisomerase I inhibitor topotecan. Thus, we here establish that inactivating terminal components of the non-homologous end-joining (NHEJ) machinery or of the BRCA1-A complex specifically confer topotecan resistance to...
Paper Details
Title
ATM orchestrates the DNA-damage response to counter toxic non-homologous end-joining at broken replication forks
Published Date
Jan 8, 2019
Volume
10
Issue
1
Pages
87 - 87
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