Biochemical reconstitution experiments uncover the ubiquitin-mediated function of a DNA repair protein, key to the understanding of Fanconi Anemia, a cancer-associated bone marrow failure syndrome.

A revised analytical framework grounded in the principle of binomial distribution captures the full clonality and dynamic shifts of hematopoiesis throughout ontogeny.

Translesion polymerase kappa promotes replication fork restart to maintain genome stability during conditions of nucleotide deprivation.

Salmonella antibacterial effectors act on Y-shaped DNA substrates resembling replication forks or transcription bubbles and lead to DNA double-strand breaks.

Cavin3 associates with BRCA1 upon disassembly of caveolae in response to mechanical and non-mechanical stressors to influence DNA repair and apoptosis.

PPM1D-mutant leukemia cells exhibit a dysregulated redox landscape, a diminished response to oxidative stress, and rely on SOD1 for their survival.

Biochemical studies revealed novel property of human tumor suppressor PALB2, which significantly contribute into DNA repair in cells and can be targeted for the development of novel anticancer treatment.

p53 suppresses genome instability by direct role at stalled replication forks for pathway regulation that explains transcription-independent p53 tumor-suppressor functions.

STAG proteins function independently of core cohesin at R-loops to facilitate cohesin loading.