Milos Dokmanovic

TL;DR: This review focuses on the activities of the 11 zinc-containing HDACs, their histone and nonhistone protein substrates, and the different pathways by which HDACi induce transformed cell death.

TL;DR: SLP induction in breast carcinoma cells treated with retinoids in vitro or in vivo was found to correlate with permanent growth inhibition under the conditions of minimal cytotoxicity, suggesting that this response may be particularly important for the antiproliferative effect of differentiating agents.

TL;DR: This review focuses on several key questions with respect to the mechanism of action of HDACi, including, what are the different cell phenotypes induced by HDAC i, why are normal cells compared to transformed cells relatively resistant toHDACi induced cell death, why is certain tumors more responsive to HDACs than others, and what is the basis of the selectivity of HDaci in altering gene expression.

TL;DR: It is found that the HDACi suberoylanilide hydroxamic acid (SAHA) and MS-275, a benzamide, cause an accumulation of reactive oxygen species (ROS) and caspase activation in transformed but not normal cells.

TL;DR: Evidence is provided that histone sumoylation is the first negative histone modification to be identified in S. cerevisiae and it is suggested thatsumoylation may serve as a general dynamic mark to oppose transcription.