During tumorigenesis loss of p53 not only abrogates cell cycle arrest and apoptosis, but also suppresses the induction of replication-stress-induced DNA double-stranded breaks.

In addition to its role in preventing tumors, the protein p53 appears to participate in a DNA repair process known as the replication-stress response.

Evolutionary adaptation to a constitutive perturbation of DNA replication reveals that adaptive mutations in three conserved pathways interact to restore faithful chromosome replication and segregation.

An investigation into 8-oxodeoxguanosine bypass by archaeal DNA polymerases.

The RIF1-long and short splice variants show distinct ability to protect cells from replication stress by promoting 53BP1 nuclear bodies, representing the first described functional difference between the two variants.

Chromatin structure is altered following DNA replication stress through the activity of protein kinase C signalling which leads to functionally coupled histone H3 phosphorylation and acetylation events.

DNA-PK and PTEN protect breast cancer cells from lethal replication stress induced by the WEE1 inhibitor AZD1775 and constitute new potential biomarkers for AZD1775 sensitivity.

The use of Research Resource Identifiers (RRIDs) improves the proper use of cell lines in the biomedical literature.