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The DNA-damage response in human biology and disease
The authors' improving understanding of DNA-damage responses is providing new avenues for disease management, and these responses are biologically significant because they prevent diverse human diseases.
Cell-cycle checkpoints and cancer
All life on earth must cope with constant exposure to DNA-damaging agents such as the Sun's radiation, and how cells respond to DNA damage are critical determinants of whether that individual will develop cancer.
Human CtIP promotes DNA end resection
These findings establish evolutionarily conserved roles for CtIP-like proteins in controlling DSB resection, checkpoint signalling and homologous recombination.
DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis
It is shown that in clinical specimens from different stages of human tumours of the urinary bladder, breast, lung and colon, the early precursor lesions commonly express markers of an activated DNA damage response.
ATM- and cell cycle-dependent regulation of ATR in response to DNA double-strand breaks
It is shown that ATM and the nuclease activity of meiotic recombination 11 are required for the processing of DNA double-strand breaks (DSBs) to generate the replication protein A (RPA)-coated ssDNA that is needed for ATR recruitment and the subsequent phosphorylation and activation of Chk1.
The ATM–Chk2–Cdc25A checkpoint pathway guards against radioresistant DNA synthesis
A functional link between ATM, the checkpoint signalling kinase Chk2/Cds1 (Chk2) and Cdc25A is reported, and this mechanism in controlling the S-phase checkpoint is identified as a genomic integrity checkpoint that prevents radioresistant DNA synthesis.
Chromatin relaxation in response to DNA double-strand breaks is modulated by a novel ATM- and KAP-1 dependent pathway
It is shown that DSB formation is followed by ATM-dependent chromatin relaxation, which suggests that chromatin Relaxation is a fundamental pathway in the DNA-damage response and identifies its primary mediators.