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Results show that deleting HDAC3 can ameliorate the impairments in both long-term memory and synaptic plasticity caused by BAF53b mutation. This suggests a dynamic interplay exists between histone acetylation/deacetylation and nucleosome remodeling mechanisms in the regulation of memory formation.
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Therefore, Hdac3 is required for iNKT cell development and differentiation.
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HDAC3 regulates multiple pathologies relevant for Alzheimer's disease. HDAC3 inhibition with RGFP-966 decreases pathological tau phosphorylation and acetylation, decreases beta-amyloid protein expression in the brain and periphery, increases beta-amyloid degradation in the periphery, and improves learning and memory in 3xTg-Alzheimer's disease mice and normalizes a number of Alzheimer's disease-related genes.
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Nptx1, Hip1r, and Hdac9 as genes whose expression is altered by HDAC3.
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This study highlights the novel mechanism of HDAC3-regulated Ucp1 expression during beta-adrenergic receptor stimulation.
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Hdac3-depletion in osteoblasts increases expression of Opg, subsequently preserving insulin sensitivity.
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HDAC3 plays an important role in regulating insulin secretion.
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Epithelial HDAC3 promotes development of diet-induced obesity in studies of mice.
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Hdac3 regulates distinct pathways in mesenchymal cell populations and is required for mesenchymal progenitor cell differentiation and long bone development.
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Results suggest that the deacetylase domain of HDAC3 plays a selective role in specific brain regions underlying long-term memory formation of object location as well as cocaine-associated memory formation and extinction.
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Reintroduction of wild-type Hdac3 restored normal B-cell development, whereas an Hdac3 point mutant lacking deacetylase activity failed to complement this defect. Thus, the deacetylase activity of Hdac3 is required for the generation of mature B cells.
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HDAC3 negatively regulates spatial memory in a mouse model of Alzheimer's disease.
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Selective HDAC3 inhibition effectively alleviated Klotho loss and kidney injury, whereas the protective effects were largely abolished when Klotho was knocked down by siRNA, suggesting that aberrant HDAC3 and Klotho loss are crucial components involved in the renal damage of mice with chronic kidney disease.
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HDAC3 deletion displayed decreased pancreatic insulin content, disrupted glucose-stimulated insulin secretion, with intermittent spontaneous diabetes and dramatically enhanced susceptibility to STZ-induced diabetes.
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Mice lacking HDAC3 in intestinal epithelial cells were more susceptible to Citrobacter rodentium. HDAC3 mediates communication between intestinal epithelial cells and resident lymphocytes.
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Hepcidin expression involves epigenetic regulation by histone deacetylase 3.
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HDAC3 interacts with PROX1.HDAC3 controls expression of genes regulating lipid homeostasis.
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Studied effect of Coptis Chinensis on glioma cells; results showed Coptis Chinensis induced cell cycle arrest and apoptosis in glioma cells, down-regulated the signal transducer and activator oftranscription 3 (STAT3) phosphorylation levels, and reduced the expression of histone deacetylase 3 (HDAC3). (HDAC3) and caspase 3.
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The authors observed that the mouse cytomegalovirus encoded protein m18 is necessary and sufficient to drive expression of the RAE-1 family of NKG2D ligands. RAE-1 is transcriptionally repressed by histone deacetylase inhibitor 3 (HDAC3) in healthy cells, and m18 relieves this repression by directly interacting with Casein Kinase II and preventing it from activating HDAC3.
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Emerin-null progenitors were delayed in their cell cycle exit, had decreased myosin heavy chain (MyHC) expression and formed fewer myotubes. Emerin binds to and activates histone deacetylase 3 (HDAC3).
