DNA double-strand breaks (DSBs) are cytotoxic lesions that threaten genome integrity and
cell viability. Typically, cells repair DSBs by either nonhomologous end joining (NHEJ) or …

DNA double-strand breaks arise accidentally upon exposure of DNA to radiation and
chemicals or result from faulty DNA metabolic processes. DNA breaks can also be …

The breast cancer susceptibility proteins BRCA1 and BRCA2 have emerged as key
stabilizing factors for the maintenance of replication fork integrity following replication stress …

The repair of DNA double-strand breaks (DSBs) by homologous recombination (HR) is
initiated by nucleolytic degradation of the 5′-terminated strands in a process termed end …

To repair double-strand DNA breaks by homologous recombination, the 5′-terminated
DNA strand must first be resected, which generates 3′ single-stranded DNA overhangs …

DNA double-strand breaks (DSBs) are cytotoxic lesions that can result in mutagenic events
or cell death if left unrepaired or repaired inappropriately. Cells use two major pathways for …

Abstract 53BP1 is an enigmatic DNA damage response factor that gained prominence
because it determines the efficacy of PARP1 inhibitory drugs (PARPi) in BRCA1-deficient …

Microhomology-mediated end joining (MMEJ) is a major pathway for Ku-independent
alternative nonhomologous end joining, which contributes to chromosomal translocations …

Accurate processing of stalled or damaged DNA replication forks is paramount to genomic
integrity and recent work points to replication fork reversal and restart as a central …

Repair of dsDNA breaks requires processing to produce 3′-terminated ssDNA. We
biochemically reconstituted DNA end resection using purified human proteins: Bloom …