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HDAC9 promotes angiogenesis and transcriptionally represses the endothelial cell miR-17-92 cluster.
HDAC9 is a target of miR (show MLXIP ELISA Kits)-377 in oral squamous cell carcinoma.
Studied HDAC9 gene's association with an increased susceptibility to acute coronary syndrome (ACS (show PLA2G15 ELISA Kits)) in Chinese Han population. The results revealed a significant association of rs2240419 with ACS (show PLA2G15 ELISA Kits) 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 (show PLA2G15 ELISA Kits) 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 (show MEF2D ELISA Kits), and NR4A1/Nur77 (show NR4A1 ELISA Kits), a pro-apoptotic MEF2 (show MEF2A ELISA Kits) target
The aurora kinase A (show AURKA ELISA Kits) inhibited by MLN (show MLN ELISA Kits) 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 (show EZH2 ELISA Kits), which silences genes by trimethylating histone H3K27.Combinations of small molecular inhibitors act synergistically in rhabdoid tumor
These results highlighting the significant correlation between TWIST and HDAC9 gene expression suggest that both genes may contribute to plaque stability in a coordinated way
Polymorphisms of HDAC9 is associated with Ischemic Stroke.
The results imply that HDAC9 is involved in the transcriptional regulation of human odontoblasts in vivo.
HDAC9 was commonly expressed in retinoblastoma tissues and HDAC9 was overexpressed in prognostically poor retinoblastoma patients.
HDAC9 promotes tumor formation of glioblastoma via TAZ (show TAZ ELISA Kits)-mediated EGFR (show EGFR ELISA Kits) pathway activation.
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 is responsible for repressing ChAT gene expression in NG108-15 neuronal cells and thus plays an important role in cholinergic differentiation.
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.
histone deacetylase 9
, histone deacetylase 9-B
, 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, MITR protein