Genetic knockout of Hdac2 modifies molecular and cellular phenotypes in Huntington’s disease mice and has a prominent transcriptional regulatory role in adult medium spiny neurons.

During heart maturation, embryonic ectoderm development as a chromatin remodeler triggers transcriptional silencing, while H3K27me3 is a passenger that is not sufficient for gene silencing.

Myelin generation during development and nerve regeneration is guaranteed by responsive backup circuits that coordinate class IIa HDACs to repress the expression of negative regulators of myelination and permit Schwann cell differentiation in response to cAMP.

Volatile compounds from microbes and food alter epigenetic states by inhibiting histone deacetylases and alter gene expression, slow degeneration in Huntington’s model flies, and slow proliferation of a neuroblastoma cell line.

Histone deacetylase 1 (Hdac1) plays a crucial role in maintaining differential histone acetylation states of enhancers in various germ layers and regulates the transcriptional program both temporally and spatially.

Viral infection can induce NKG2D ligand expression through the action of virally encoded histone deacetylase (HDAC) inhibitors, which release HDAC mediated repression of NKG2D ligands.

By analyzing five purified recombinant histone deacetylase complexes and designer acetylated mononucleosome substrates, the molecular basis of the unusual substrate specificity of the CoREST complex was revealed.

A functional ovarian-specific PAX8-centric regulon is susceptible to FDA-approved HDAC inhibitors, providing the rationale to target human cancers driven by lineage-survival oncogenes with epigenetic therapeutics perturbing the enhancer topology.

A versatile acetylation-methylation switch at lysine 31 on the lateral surface of histone H4 contributes to chromatin structure in apicomplexan parasites.

HDAC3 regulates the development of pDCs and maintenance of homeostasis of hematopoietic progenitors with dendritic cell (DC) differentiation potential, mechanistically by repressing cDC1 associated genes in a deacetylase-dependent manner.