Yves Pommier

TL;DR: The study reveals that human myeloblastic leukemia HL60 and K562 and colon carcinoma HT29 cells undergo internucleosomal DNA fragmentation and morphological changes characteristic of apoptosis after UCN-01 treatment, and demonstrates that the protein kinase C inhibitor and antitumor agent, UCn-01 is a potent apoptosis inducer in cell lines that are usually resistant to apoptosis.

TL;DR: It is reported that BLM-deficient cell lines and primary fibroblasts display an endogenously activated DNA double-strand break checkpoint response with prominent levels of phosphorylated histone H2AX, ATM, and Chk2 colocalizing in nuclear foci.

TL;DR: TDP1 seems to be critical for repairing nuclear and mitochondrial DNA damage caused by CTNAs, and it is shown that Tdp1−/− cells are hypersensitive and accumulate more DNA damage when treated with ACV and Ara-C, implicating TDP1 in repairing CTNA-induced DNA damage.

TL;DR: To organize the rapidly accumulating information on bioregulatory networks related to the histone γ-H2AX-ATM-Chk2-p53-Mdm2 pathways in concise and unambiguous diagrams, the molecular interaction map notation is used (http://discover.nci.nih.gov/min).

TL;DR: The compensation mechanism described here contributes to the survival of Top1mt−/− cells and mice despite alterations of mitochondrial functions and metabolism, and supports a novel model for cellular adaptation to mitochondrial damage.