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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).
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Hdac3 is a key epigenetic modifier that maintains blood-lymph separation and integrates both extrinsic forces and intrinsic cues to regulate lymphatic valve development.
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HDAC3 controls the temporal and spatial expression of tissue-remodeling genes and inflammatory responses in chondrocytes to ensure proper endochondral ossification during development.
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HDAC3, through deacetylating tubulin, promotes microtubule stability and the establishment of kinetochore-microtubule interaction, consequently ensuring proper spindle morphology, accurate chromosome movement and orderly meiotic progression during oocyte maturation
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These studies showed that HDAC3 regulates WAT metabolism by activating a futile cycle of fatty acid synthesis and oxidation, which supports WAT browning.
