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Brm-HDAC3-Erm repressor complex suppresses dedifferentiation of intermediate neural progenitors back into type II neuroblasts.
Hdac3 served as an important regulator of the PI3K pathway and revealed a novel link between histone acetylation and growth control.
Overexpressing any of HDAC 3, 6, or 11 suppresses CGG repeat-induced neurodegeneration in a Drosophila model of fragile X tremor ataxia syndrome.
) DHDAC1 (show HDAC1 ELISA Kits) and -3 have distinct functions in the control of gene expression
Mutant larvae display small imaginal discs, which result from abnormally elevated levels of apoptosis. This cell death occurs as a cell-autonomous response to HDAC3 loss and is accompanied by increased expression of the pro-apoptotic gene, hid.
Knockdown of either Xist or SPEN (show SPEN ELISA Kits) expression in breast cancer cells suppressed the expression of PHLPP1 (show PHLPP1 ELISA Kits), a phosphatase in AKT (show AKT1 ELISA Kits) dephosphorylation, and was correlated with increased HDAC3 recruitment to the PHLPP1 (show PHLPP1 ELISA Kits) promoter.
Data show that BRCA2 was required for HDAC2/3 association with acetylated BubR1 in nocodazole (Noc)-arrested cells.
Data show that the nuclear HDAC3 and cytoplasmic CDH1 (show CDH1 ELISA Kits) have independent prognostic value in pancreatic cancer and provide targets for prognostic therapeutics.
HDAC3 uniquely primes Ucp1 (show UCP1 ELISA Kits) and the thermogenic transcriptional program to maintain a critical capacity for thermogenesis in brown adipose tissue that can be rapidly engaged upon exposure to dangerously cold temperature
The low expression of HDAC3 and overexpession of inflammatory cytokines (IL-18 (show IL18 ELISA Kits), IL-12 (show IL12A ELISA Kits) and TNF-alpha (show TNF ELISA Kits)) in intrahepatic cholestasis of pregnancy may be involved in liver cell apoptosis and in the pathophysiology of the disease.
SNP rs14251 was found to be significant (and rs2530223 to be nominally significantly associated with the increasing risk of SCZ susceptibility in Han Chinese individuals, suggesting this gene as a potential genetic modifier for SCZ development.
Inhibition of HDAC3 with targeted therapy could benefit treatment of the diseases associated with sGCbeta1 down-regulation and/or deficiency such as cancer and several vascular-related diseases.
that histone deacetylase 3 interaction with MeCP2 positively regulates a subset of neuronal genes through FOXO (show FOXO3 ELISA Kits) deacetylation, and disruption of HDAC3 contributes to cognitive and social impairment
provide evidence to show that CBX4 may serve as a tumor suppressor in colorectal carcinoma by recruiting HDAC3 to the Runx2 (show RUNX2 ELISA Kits) promoter to impede Runx2 (show RUNX2 ELISA Kits) expression
miRNA1236 regulates hypoxia-induced epithelial-mesenchymal transformation and metastasis by repressing HDAC3 and SENP1 (show SENP1 ELISA Kits) expression.
HDAC3 interacts with PROX1.HDAC3 controls expression of genes regulating lipid homeostasis.
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 (show STAT3 ELISA Kits)) phosphorylation levels, and reduced the expression of histone deacetylase 3 (HDAC3). (HDAC3) and caspase 3 (show CASP3 ELISA Kits).
The authors observed that the mouse cytomegalovirus encoded protein m18 is necessary and sufficient to drive expression of the RAE-1 (show RAE1 ELISA Kits) family of NKG2D (show KLRK1 ELISA Kits) ligands. RAE-1 (show RAE1 ELISA Kits) is transcriptionally repressed by histone deacetylase (show HDAC1 ELISA Kits) inhibitor 3 (show PPP1R11 ELISA Kits) (HDAC3) in healthy cells, and m18 relieves this repression by directly interacting with Casein Kinase II (show CSNK2A1 ELISA Kits) and preventing it from activating HDAC3.
Emerin (show EMD ELISA Kits)-null progenitors were delayed in their cell cycle exit, had decreased myosin heavy chain (MyHC) expression and formed fewer myotubes. Emerin (show EMD ELISA Kits) binds to and activates histone deacetylase 3 (HDAC3).
Hdac3 is a key epigenetic modifier that maintains blood-lymph separation and integrates both extrinsic forces and intrinsic cues to regulate lymphatic valve development.
HDAC3 controls the temporal and spatial expression of tissue-remodeling genes and inflammatory responses in chondrocytes to ensure proper endochondral ossification during development.
HDAC3, through deacetylating tubulin (show TUBB ELISA Kits), 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
These studies showed that HDAC3 regulates WAT metabolism by activating a futile cycle (show LRMP ELISA Kits) of fatty acid synthesis and oxidation, which supports WAT browning.
Hdac3 tethers peripheral heterochromatin containing lineage-relevant genes to the nuclear lamina. Deletion of Hdac3 in cardiac progenitor cells releases genomic regions from the nuclear periphery, leading to precocious cardiac gene expression and differentiation into cardiomyocytes; in contrast, restricting Hdac3 to the nuclear periphery rescues myogenesis in progenitors otherwise lacking Hdac3.
These in vivo results point to the potential use of selective HDAC3 inhibitors as a therapeutic approach to suppress pancreatic islet infiltration and prevent beta-cell death with the long-term goal of limiting the progression of type 1 diabetes.
These results revealed a novel and specific role of hdac3 in liver development and the distinct functions between hdac1 (show HDAC1 ELISA Kits) and hdac3 in zebrafish embryonic development.
Histones play a critical role in transcriptional regulation, cell cycle progression, and developmental events. Histone acetylation/deacetylation alters chromosome structure and affects transcription factor access to DNA. The protein encoded by this gene belongs to the histone deacetylase/acuc/apha family. It has histone deacetylase activity and represses transcription when tethered to a promoter. It may participate in the regulation of transcription through its binding with the zinc-finger transcription factor YY1. This protein can also down-regulate p53 function and thus modulate cell growth and apoptosis. This gene is regarded as a potential tumor suppressor gene.
, histone Deacetylase-3
, histone deacetylase 3
, HDAC3 splicing HDAC3alpha
, HDAC3 splicing HDAC3beta
, HDAC3 splicing HDAC3delta
, HDAC3 splicing HDAC3gamma
, histone deacetylase-3