Giacomo Buscemi

TL;DR: The activity of CHK2 in response to DNA damage and in the maintenance of the biological functions in unstressed cells are discussed and their activities are considered in relation to a possible role of CHk2 in tumorigenesis and, as a consequence, in the target of cancer therapy.

TL;DR: It is shown that the ATM-dependent activation of Chk2 by γ- radiation requires Nbs1, the gene product involved in the Nijmegen breakage syndrome (NBS), a disorder that shares with AT a variety of phenotypic defects including chromosome fragility, radiosensitivity, and radioresistant DNA synthesis, and suggest that checkpoint defects in NBS cells may result from the inability to activate Chk1.

TL;DR: The results indicate that, in contrast to ATM, Chk2 activity is triggered by a greater number of DSBs, implying that, below a certain threshold level of lesions, DNA repair can occur through ATM, without enforcing Chk1-dependent checkpoints.

TL;DR: A new family with two affected siblings, ATLD5 and ATLD6, now aged 37 and 36, respectively, are described, demonstrating the interconnection between ATM activity and MRN function, which rationalizes the clinical similarity between ataxia-telangiectasia (A-T) and AT LD.

TL;DR: The data indicate that binding of a 14-3-3 dimer and subsequent nuclear accumulation are essential steps toward degradation of p53's inhibitor, Hdmx, in response to DNA damage.