DNA double-strand break (DSB) signalling and repair is crucial to preserve genomic
integrity and maintain cellular homeostasis. p53-binding protein 1 (53BP1) is an important …

DNA double-strand breaks (DSBs) are highly toxic lesions that can drive genetic instability.
To preserve genome integrity, organisms have evolved several DSB repair mechanisms, of …

Abstract 53BP1 is a chromatin-binding protein that regulates the repair of DNA double-
strand breaks by suppressing the nucleolytic resection of DNA termini,. This function of …

Repair of damaged DNA is essential for maintaining genome integrity and for preventing
genome-instability-associated diseases, such as cancer. By combining proximity labeling …

BRCA1 deficiencies cause breast, ovarian, prostate and other cancers, and render tumours
hypersensitive to poly (ADP-ribose) polymerase (PARP) inhibitors. To understand the …

Cells deficient in the Brca1 and Brca2 genes have reduced capacity to repair DNA double-
strand breaks by homologous recombination and consequently are hypersensitive to DNA …

G-quadruplex DNAs form four-stranded helical structures and are proposed to play key roles
in different cellular processes. Targeting G-quadruplex DNAs for cancer treatment is a very …

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 …

DNA double-strand breaks (DSBs) are highly cytotoxic DNA lesions. The swift recognition
and faithful repair of such damage is crucial for the maintenance of genomic stability, as well …

DNA double-strand break (DSB) repair pathway choice is governed by the opposing
activities of 53BP1 and BRCA1. 53BP1 stimulates nonhomologous end joining (NHEJ) …