Norikazu Nishino

TL;DR: FK228 serves as a stable prodrug to inhibit class I enzymes and is activated by reduction after uptake into the cells and implicates its clinical usefulness for counteracting glutathione-mediated drug resistance in chemotherapy.

TL;DR: It is suggested that acetylation and deacetylation are coupled to the microtubule turnover and that HDAC6 plays a key regulatory role in the stability of the dynamic microtubules.

TL;DR: Interestingly, HDAC6, but not HDAC1 or HDAC4, was resistant to TPX and CHAP1, whereas TSA inhibited these HDACs to a similar extent, indicating that the structure of the cyclic tetrapeptide framework affects the target enzyme specificity.

TL;DR: The results demonstrate that the level of Runx2 is controlled by a dynamic equilibrium of acetylation, deacetylations, and ubiquitination, in BMP signaling.

TL;DR: CHAP31, the strongest HDAC inhibitor obtained from a variety of CHAP derivatives, exhibited antitumor activity in BDF1 mice bearing B16/BL6 tumor cells, suggesting that CHAP31 is promising as a novel therapeutic agent for cancer treatment, and thatCHAP may serve as a basis for new HDAC inhibitors and be useful for combinatorial synthesis and high-throughput screening.