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

Abstract excerpt

ATR kinase activity slows replication forks and prevents origin firing in damaged cells. Here we describe proteomic analyses that identified mechanisms through which ATR kinase inhibitors induce unscheduled origin firing in undamaged cells. ATR-Chk1 inhibitor-induced origin firing is mediated by Cdc7 kinase through previously undescribed phosphorylations on GINS that induce an association between GINS and And-1....

Topics

Share this publication in a Topic to start or enrich a Post.

• Share to Cancer-related Molecular Pathways
• Share to DNA Repair Mechanisms
• Share to Microtubule and mitosis dynamics