Loss of SIM2s inhibits RAD51 binding and leads to unresolved replication stress.

ABSTRACT:

Background

Mutations in genes associated with homologous recombination (HR) increase an individual's risk of developing triple-negative breast cancer (TNBC). Although known for their role in repairing dsDNA breaks, HR repair elements also stabilize and restart stalled replication forks. Essential to these functions are RAD51 and its paralogs, each of which has a unique role in preventing replication fork collapse and restart. However, progress toward understanding the regulation of these factors has been slow. With such a pivotal role in the maintenance of genomic integrity, furthering our understanding of this pathway through the discovery of new factors involved in HR is important. Recently, we showed that singleminded-2s (SIM2s) is stabilized in response to dsDNA breaks and is r

SUBMITTER: Pearson SJ 

PROVIDER: S-EPMC6882179 | biostudies-literature | 2019 Nov

REPOSITORIES: biostudies-literature