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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.
Oncogene-induced senescence is part of the tumorigenesis barrier imposed by DNA damage checkpoints
It is shown that oncogene-induced senescence is associated with signs of DNA replication stress, including prematurely terminated DNA replication forks and DNA double-strand breaks, and, together with apoptosis, provides a barrier to malignant progression.
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.
Rapid destruction of human Cdc25A in response to DNA damage.
These results identify specific degradation of Cdc25A as part of the DNA damage checkpoint mechanism and suggest how CDC25A overexpression in human cancers might contribute to tumorigenesis.