Sustained E2F-Dependent Transcription Is a Key Mechanism to Prevent Replication-Stress-Induced DNA Damage
E2F
Transcription
DOI:
10.1016/j.celrep.2016.04.036
Publication Date:
2016-05-05T18:09:48Z
AUTHORS (5)
ABSTRACT
Recent work established DNA replication stress as a crucial driver of genomic instability and key event at the onset cancer. Post-translational modifications play an important role in cellular response to by regulating activity components prevent replication-stress-induced damage. Here, we establish far greater for transcriptional control determining outcome events than previously suspected. Sustained E2F-dependent transcription is both required sufficient many checkpoint functions, including fork stalling, stabilization, resolution. Importantly, also find that, context oncogene-induced stress, where increased E2F thought cause limit levels These data suggest model which cells experiencing through deregulation become addicted cope with high stress.
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