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
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.
SUPPLEMENTAL MATERIAL
Coming soon ....
REFERENCES (27)
CITATIONS (57)