Shannon E. Mullican

TL;DR: It is shown that genomic recruitment of HDAC3 by Rev-erbα directs a circadian rhythm of histone acetylation and gene expression required for normal hepatic lipid homeostasis.

TL;DR: These findings establish the two Rev-erbs as major regulators of both clock function and metabolism, displaying a level of subtype collaboration that is unusual among nuclear receptors but common among core clock proteins, protecting the organism from major perturbations in circadian and metabolic physiology.

TL;DR: A critical role is demonstrated for HDAC3 in the molecular mechanisms underlying long-term memory formation in mice modified with adeno-associated virus-expressing Cre recombinase and a selective inhibitor ofHDAC3 via RGFP136.

TL;DR: It is shown that specific, genetic disruption of the Ncor1–Hdac3 interaction in mice causes aberrant regulation of clock genes and results in abnormal circadian behaviour, demonstrating that circadian regulation of metabolism is critical for normal energy balance.

TL;DR: It is reported that macrophages lacking histone deacetylase 3 (HDAC3) display a polarization phenotype similar to IL-4-induced alternative activation and, furthermore, are hyperresponsive to IL (IL-4) stimulation.