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M4 macrophages are a possible source for HDAC9 and MMP12 (show MMP12 ELISA Kits) expression in advanced human carotid plaques.
HDAC9 is an important epigenetic factor regulating ox-LDL-induced endothelial cell apoptosis and inflammatory factor expression.
decline in HDAC9c expression over time was accompanied by increased EZH2 (show EZH2 ELISA Kits) expression.
HDAC9 might contribute to lymphomagenesis by altering pathways involved in growth and survival, as well as modulating BCL6 (show BCL6 ELISA Kits) activity and p53 tumor suppressor (show TP53 ELISA Kits) function.
post-translational modification of Nkx3.2 (show NKX3-2 ELISA Kits) employing HDAC9-PIASy (show PIAS4 ELISA Kits)-RNF4 (show RNF4 ELISA Kits) axis plays a crucial role in controlling chondrocyte viability and hypertrophic maturation during skeletal development in vertebrates.
Data show that the gene encoding the transcription factor SOX9 (show SOX9 ELISA Kits) was identified by a global transcriptomic approach as an HDAC9 target gene.
The minor allele A of SNP rs2107595 increased coronary artery disease risk and the severity of coronary atherosclerosis in a Chinese Han population.
in leiomyosarcomas (LMS), this two-faced trait of MEF2 (show MEF2A ELISA Kits) is relevant for tumor aggressiveness. Class IIa HDACs are overexpressed in 22% of LMS, where high levels of MEF2 (show MEF2A ELISA Kits), HDAC4 (show HDAC4 ELISA Kits) and HDAC9 inversely correlate with overall survival. The knock out of HDAC9 suppresses the transformed phenotype of LMS cells, by restoring the transcriptional proficiency of some MEF2 (show MEF2A ELISA Kits)-target loci
Based on this study, it is suggested that HDAC9 regulates the formation of APBs and could be a candidate for the target of ALT-cancer therapy.
PC3/Tis21 (show BTG2 ELISA Kits) associates with HDAC1 (show HDAC1 ELISA Kits), HDAC4 (show HDAC4 ELISA Kits), and HDAC9 in vivo, in fibroblast cells.
Xenograft study in nude mice showed that downregulation of HDAC9 inhibited tumor growth and development in vivo.
Dach2 (show DACH2 ELISA Kits) and Hdac9 mediate the effects of muscle activity on muscle reinnervation; Myog (show MYOG ELISA Kits) and Gdf5 (show GDF5 ELISA Kits) appear to stimulate muscle reinnervation through parallel pathways
HDAC9 is a novel, important and physiologically relevant modulator of bone remodeling and skeletal homeostasis.
Class IIa HDAC9 interact with Class IIb HDAC6 to modulate cell movement and survival in GnRH neurons
Compared with HDAC9(+/+)ApoE (show APOE ELISA Kits)(-/-) mice, HDAC9(-/-)ApoE (show APOE ELISA Kits)(-/-) mice exhibited markedly reduced lesion sizes throughout atherosclerotic aortas and significantly less advanced lesions.
HDAC9 deletion decreased atherosclerosis in LDLr (show LDLR ELISA Kits)(-/-) mice with minimal effect on plasma lipids. Macrophage HDAC9 upregulation is atherogenic via suppression of cholesterol efflux and generation of alternatively activated macrophages in atherosclerosis.
Genetic ablation of HDAC9 improves adipogenic differentiation and systemic metabolic state during a high-fat diet, resulting in diminished weight gain, improved glucose tolerance and insulin (show INS ELISA Kits) sensitivity, and reduced hepatosteatosis.
Dephosphorylation at a conserved SP motif governs cAMP sensitivity and nuclear localization of class IIa histone deacetylases HDAC4 (show HDAC5 ELISA Kits), 5 and 9
HDAC9 promotes angiogenesis and transcriptionally represses the endothelial cell miR-17-92 cluster.
The authors found that HDA9 acts in complex with a SANT domain-containing protein POWERDRESS (PWR) and transcription factor WRKY53. Genome-wide profiling of HDA9 occupancy reveals that HDA9 directly binds to the promoters of key negative regulators of senescence and this association requires PWR.
HDA9 might be a novel chromatin protein that negatively regulates plant sensitivity to salt and drought stresses.
HDA9 prevents precocious flowering under SD conditions by curbing the hyperactivation of AGL19, an upstream activator of FT, through resetting the local chromatin environment.
HDA9 negatively influences germination and is involved in the suppression of seedling traits in dry seeds, probably by transcriptional repression via histone deacetylation.
The data indicate thatHDA9 represses flowering by repressing AGL19 gene expressionindependently of CONSTANS or FLC pathways.
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 has sequence homology to members of the histone deacetylase family. This gene is orthologous to the Xenopus and mouse MITR genes. The MITR protein lacks the histone deacetylase catalytic domain. It represses MEF2 activity through recruitment of multicomponent corepressor complexes that include CtBP and HDACs. This encoded protein may play a role in hematopoiesis. Multiple alternatively spliced transcripts have been described for this gene but the full-length nature of some of them has not been determined.
MEF-2 interacting transcription repressor (MITR) protein
, histone deacetylase 4/5-related protein
, histone deacetylase 7B
, MEF2-interacting transcription repressor MITR
, histone deacetylase-related protein
, histone deacetylase 9
, histone deacetylase 9-B
, histone deacetylase 9, MITR protein
, LOW QUALITY PROTEIN: histone deacetylase 9