DNA double‐strand breaks are a threat to genome integrity and cell viability. The nucleolytic
processing of broken DNA ends plays a central role in dictating the repair processes that will …

Life as we know it, simply would not exist without DNA replication. All living organisms utilize
a complex machinery to duplicate their genomes and the central role in this machinery …

Abstract 53BP1 governs a specialized, context-specific branch of the classical non-
homologous end joining DNA double-strand break repair pathway. Mice lacking 53bp1 (also …

Error-free repair of DNA double-strand breaks (DSBs) is achieved by homologous
recombination (HR), and BRCA1 is an important factor for this repair pathway. In the …

Oncogene activation creates DNA replication stress (RS) in cancer cells, which can
generate under-replicated DNA regions (UDRs) that persist until cells enter mitosis. UDRs …

Appropriate repair of DNA lesions and the inhibition of DNA repair activities at telomeres are
crucial to prevent genomic instability. By fuelling the generation of genetic alterations and by …

During eukaryotic cell division, the sister chromatids of duplicated chromosomes are pulled
apart by microtubules, which connect via kinetochores. The kinetochore is a multiprotein …

DNA double-strand breaks (DSBs) are repaired through homology-directed repair (HDR) or
non-homologous end joining (NHEJ). BRCA1/2-deficient cancer cells cannot perform HDR …

The eukaryotic replicative DNA polymerases (Pol α, δ and ɛ) and the major DNA
mutagenesis enzyme Pol ζ contain two conserved cysteine-rich metal-binding motifs (CysA …

The maintenance of genome stability is critical for survival, and its failure is often associated
with tumorigenesis. The Fanconi anemia (FA) pathway is essential for the repair of DNA …