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Human Polyclonal HDAC9 Primary Antibody for IF, IHC (p) - ABIN387960
Petrie, Guidez, Howell, Healy, Waxman, Greaves, Zelent: The histone deacetylase 9 gene encodes multiple protein isoforms. in The Journal of biological chemistry 2003
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Human Polyclonal HDAC9 Primary Antibody for WB - ABIN223304
Maltepe, Krampitz, Okazaki, Red-Horse, Mak, Simon, Fisher: Hypoxia-inducible factor-dependent histone deacetylase activity determines stem cell fate in the placenta. in Development (Cambridge, England) 2005
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Human Polyclonal HDAC9 Primary Antibody for IF, IHC (p) - ABIN543300
Mahlknecht, Schnittger, Will, Cicek, Hoelzer: Chromosomal organization and localization of the human histone deacetylase 9 gene (HDAC9). in Biochemical and biophysical research communications 2002
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Human Polyclonal HDAC9 Primary Antibody for IHC (p), IP - ABIN543301
David, Cardoso, Marques, Marques, Silva, Santos, Boavida: Molecular characterization of a familial translocation implicates disruption of HDAC9 and possible position effect on TGFbeta2 in the pathogenesis of Peters' anomaly. in Genomics 2003
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Guinea Pig Polyclonal HDAC9 Primary Antibody for ChIP, IHC - ABIN2775576
Han, He, Wu, Liu, Chen: Mechanism of recruitment of class II histone deacetylases by myocyte enhancer factor-2. in Journal of molecular biology 2004
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Human Polyclonal HDAC9 Primary Antibody for IHC (p), WB - ABIN387961
Zhou, Marks, Rifkind, Richon: Cloning and characterization of a histone deacetylase, HDAC9. in Proceedings of the National Academy of Sciences of the United States of America 2001
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Cow (Bovine) Polyclonal HDAC9 Primary Antibody for WB - ABIN2775579
Su, Becker, Kozyrskyj, Hayglass: Epigenetic regulation of established human type 1 versus type 2 cytokine responses. in The Journal of allergy and clinical immunology 2008
HDAC [histone deacetylases] may be involved in the pathogenesis of COP [cryptogenic organizing pneumonia] and IPF [idiopathic pulmonary fibrosis].
The HDAC9 risk allele at rs2107595 was associated with differences in blood cell gene expression in patients with Large Vessel Atherosclerotic Stroke.
the key role of the HDAC9-FoxO1 signalling axis in regulating gluconeogenic genes, transcriptional factors, gluconeogenesis metabolism, and HCV-induced gluconeogenesis in hepatocytes.
HDAC9 polymorphisms are associated with susceptibility, severity, and short-term outcome of large artery atherosclerotic stroke.
This study highlights HDAC9 as a mediator of cell invasion and angiogenesis in Triple negative breast cancer (TNBC) cells through VEGF and MAPK3 by modulating miR-206 expression and suggests that selective inhibition of HDAC9 may be an efficient route for TNBC therapy.
the T allele of rs2107595 in HDAC9 increases the risk of stroke but that the G allele of rs2389995 decreases the risk of stroke in the Chinese population (Meta-Analysis)
HDAC9 may be a new indicator for assessing chronic heart failure.
HDAC9 may be involved in the process of diabetic nephropathy.
HDAC9, in cooperation with BRG1 and MALAT1, mediates a critical epigenetic pathway responsible for vascular smooth muscle cells dysfunction.
M4 macrophages are a possible source for HDAC9 and MMP12 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 expression.
HDAC9 might contribute to lymphomagenesis by altering pathways involved in growth and survival, as well as modulating BCL6 activity and p53 tumor suppressor function.
post-translational modification of Nkx3.2 employing HDAC9-PIASy-RNF4 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 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 is relevant for tumor aggressiveness. Class IIa HDACs are overexpressed in 22% of LMS, where high levels of MEF2, HDAC4 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-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 associates with HDAC1, HDAC4, and HDAC9 in vivo, in fibroblast cells.
HDAC9 is a target of miR-377 in oral squamous cell carcinoma.
miR-182 upregulates LPL expression, promotes lipid accumulation in atherosclerotic lesions, and increases proinflammatory cytokine secretion, likely through targetingHDAC9, leading to an acceleration of atherogenesis in ApoE-KO mice.
HDAC9 depletion resulted in a decreased infarct volume and an improved neurological function in mice after ischemic reperfusion (I/R) injury.
Xenograft study in nude mice showed that downregulation of HDAC9 inhibited tumor growth and development in vivo.
Dach2 and Hdac9 mediate the effects of muscle activity on muscle reinnervation; Myog and Gdf5 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(-/-) mice, HDAC9(-/-)ApoE(-/-) mice exhibited markedly reduced lesion sizes throughout atherosclerotic aortas and significantly less advanced lesions.
HDAC9 deletion decreased atherosclerosis in LDLr(-/-) 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 sensitivity, and reduced hepatosteatosis.
Dephosphorylation at a conserved SP motif governs cAMP sensitivity and nuclear localization of class IIa histone deacetylases HDAC4, 5 and 9
HDAC9 promotes angiogenesis and transcriptionally represses the endothelial cell miR-17-92 cluster.
HDAC9 is responsible for repressing ChAT gene expression in NG108-15 neuronal cells and thus plays an important role in cholinergic differentiation.
Data indicate that although histone deacetylases HDAC6, HDAC9, and Sirt1 all deacetylated Foxp3, each protein had different effects on transcription factors that control expression of the gene encoding Foxp3.
investigation of role of class IIa HDAC isoenzymes in pancreas development: Data suggest HDAC4, -5, and -9 are key regulators controlling the pancreatic beta-/delta-cell lineage.
HDAC9 acts as an epigenetic switch in effector T cell-mediated systemic autoimmunity.
findings provide new insights into mechanisms of adipogenic differentiation and document a critical regulatory role for HDAC9 in adipogenic differentiation through a deacetylase-independent mechanism
Histone deacetylase 9 (HDAC9) regulates the functions of the ATDC (TRIM29) protein
POWERDRESS (PWR) acts as a subunit in a complex with HDA9 to result in lysine deacetylation of histone H3 at specific genomic targets
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