CBP/EP300 bromodomain inhibitors have a therapeutic application in oncology via targeting the IRF4 transcriptional program, a clinically validated network critical for multiple myeloma cell viability.

A method for measuring p300 chromatin occupancy in specific lineages of mouse tissues was used to map endothelial enhancers and to identify previously unrecognized angiogenesis-related sequence motifs.

At most physiological concentrations, the short-chain fatty acids propionate and butyrate affect histone acetylation by modifying and activating the acetyltransferase p300/CBP, rather than by inhibiting histone deacetylases.

A normally cytoplasmic deacetylase, Hdac6, localizes to the nucleus in embryonic stem cells, where it regulates the essential Tip60-p400 chromatin remodeling complex.

The decrease in alpha rhythm amplitude in the parietal regions after the presentation of a deviant auditory stimulus gives rise to a part of the P300-evoked response.

Ultrasonic neurostimulation in humans can manipulate response inhibition related behavior and neural activity.

CBP/p300 acetylation of histone H3 at promoters and enhancers stimulates transcriptional elongation through recruitment of the super-elongation complex and BRD4.

Definition of leukemia gene expression mechanisms reveals general principles of cancer gene control and offers a pharmacologic strategy for its therapeutic reprogramming.

Salicylic acid, the precursor to aspirin, is an anti-tumor agent that blocks protein acetylation.

A long non-coding RNA removes the transcriptional repressor p50 to regulate recruitment of co-activator p300 and RNA Polymerase II complexes to activate the COX-2 gene in human mammary epithelial cells and macrophages.