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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.
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.
class I HDACs (HDAC1 (show HDAC1 ELISA Kits), 2, 3 and 8) play a major role in regulating extracellular matrix and Epithelial-mesenchymal transition, whereas class IIa HDACs (HDAC4 (show HDAC4 ELISA Kits) and 5) are less effective.
Histone deacetylase 3 regulates the inflammatory gene expression programme of rheumatoid arthritis fibroblast-like synoviocytes.
Study demonstrated an association of elevated HDAC3 activity and HDAC3 mRNA expression in patients with type 2 diabetes (T2DM) which was positively correlated with proinflammation and insulin (show INS ELISA Kits) resistance.
HDAC3 upregulation is associated with hepatocellular carcinoma.
High HDAC3 expression is associated with pancreatic cancer.
depletion of the epigenome modifier histone deacetylase 3 (HDAC3) specifically in skeletal muscle causes severe systemic insulin (show INS ELISA Kits) resistance in mice but markedly enhances endurance and resistance to muscle fatigue, despite reducing muscle force. This is due to lower glucose utilization and greater lipid oxidation in HDAC3-depleted muscles, a fuel switch caused by the activation of anaplerotic reactions driven by Ampd3 (show AMPD3 ELISA Kits).
Mice lacking Hdac 3 specifically in the developing lung mesenchyme display lung hypoplasia including decreased mesenchymal proliferation and a severe impairment of AT1 (show SLC33A1 ELISA Kits) cell differentiation. This is correlated with a decrease in Wnt (show WNT2 ELISA Kits)/beta-catenin (show CTNNB1 ELISA Kits) signaling in the lung epithelium.
we found that histone deacetylase (HDAC (show HDAC1 ELISA Kits)) 3 is required for T cell development
Hdac3 controls the temporal and spatial expression of tissue-remodeling genes in chondrocytes to ensure proper endochondral ossification during development.
These results demonstrate that HDAC3 and SCAP control symbiotic pathways of liver lipid metabolism that are critical for suppression of lipotoxicity.
The study describes an interaction network of STAT5a (show STAT5A ELISA Kits)/LSD1 (show KDM1A ELISA Kits)/HDAC3 and a dual function of LSD1 (show KDM1A ELISA Kits)/HDAC3 on STAT5a (show STAT5A ELISA Kits)-dependent transcription, defined by protein-protein interactions, genomic binding localization/affinity and motifs.
Both the acetylation and SUMOylation status of the PXR protein is affected by its ability to associate with the lysine de-acetylating enzyme HDAC3 in a complex with SMRT.
The present study provides the first critical in vivo evidence showing a causal link between epigenetic modification of miR (show MLXIP ELISA Kits)-10a mediated by HDAC3 and the development of diabetic nephropathy, and these results elucidate that HDAC3/miR (show MLXIP ELISA Kits)-10a/CREB1 (show CREB1 ELISA Kits) serves as a new mechanism underlying kidney injury, providing potential therapeutic targets in type 2 diabetes
Hdac3 induces an medullary thymic epithelial cells-specific transcriptional program.
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