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.

Meiotic cells inhibit two distinct steps of replisome assembly with multiple kinases to prevent DNA replication between Meiosis I and Meiosis II.

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.

Nucleosomal DNAs assembled or modified by different chromatin remodeling enzymes differentially impact the origin licensing and helicase activation steps of replication initiation.

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