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Cell cycle arrest in response to a double-stranded break is initially maintained by the DNA damage checkpoint and later by the spindle assembly checkpoint.

The involvement of SETD2 in an important DNA repair pathway could explain the high frequency of SETD2 mutations in several cancers and may provide an alternative mechanism to evade the p53-mediated checkpoint.

Genome-wide mapping of heteroduplex DNA (a recombination intermediate) formed during mitotic recombination in yeast demonstrates that the "classical" model of double-strand DNA break repair is inadequate to explain several aspects of mitotic recombination.

Structural and biochemical analysis of human CtIP provides new insights into DNA break recognition, binding and bridging during homologous recombination.

Polymerase θ is among the most proficient terminal transferases known and switches between three different mechanisms of terminal transferase activity.

A DNA–protein complex can find target sequences of bases in another DNA molecule by sliding along it.

Progressive changes in Purkinje neuron perturbations and overall cerebellar atrophy correlate for the first time with the development of an overt loss of motor function in a novel mouse model of Ataxia Telangiectasia.

Building on previous work (Wilkinson et al, 2016), it is shown that inhibition of RecBCD-induced DNA break repair can be used as a co-antibacterial strategy with quinolones.

X-ray crystallography reveals that the Dna2 nuclease-helicase contains a long tunnel through which single-stranded DNA threads, and an allosteric mechanism for displacing the DNA-binding protein Rpa that restricts cleavage to the proper polarity.

Platinum chemotherapy resistance is a complex process involving multiple signalling pathways and a novel, non-genetic, cell cycle-dependent mechanism that promotes tumour regrowth and highlights potential complications for combination therapies in human lung adenocarcinoma.