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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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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 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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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
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.
Studied HDAC9 gene's association with an increased susceptibility to acute coronary syndrome (ACS) in Chinese Han population. The results revealed a significant association of rs2240419 with ACS risk in which the A allele (P = 0.047) and the A allele carriers (AA + AG) (P = 0.037) were more likely to be in ACS group as compared to those in the control group.
Downregulation of HDAC9 promotes gliomas.
overexpression of HDAC9 contributes to OSCC carcinogenesis via targeting a transcription factor, MEF2D, and NR4A1/Nur77, a pro-apoptotic MEF2 target
The aurora kinase A inhibited by MLN 8054 are both implicated in cell cycle progression and, thus, in cellular proliferation.Epigenetic regulators were targeted by SAHA inhibiting HDACs and by DZNep inhibiting the histone methyltransferase EZH2, which silences genes by trimethylating histone H3K27.Combinations of small molecular inhibitors act synergistically in rhabdoid tumor
HDAC9 promotes angiogenesis and transcriptionally represses the endothelial cell miR-17-92 cluster.
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