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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 (show HDAC9 ELISA Kits) inversely correlate with overall survival. The knock out of HDAC9 (show HDAC9 ELISA Kits) 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 (show HDAC9 ELISA Kits) in vivo, in fibroblast cells.
HDAC9 (show HDAC9 ELISA Kits) is a target of miR (show MLXIP ELISA Kits)-377 in oral squamous cell carcinoma.
Studied HDAC9 (show HDAC9 ELISA Kits) 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 (show HDAC9 ELISA Kits) promotes gliomas.
overexpression of HDAC9 (show HDAC9 ELISA Kits) 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 (show HDAC9 ELISA Kits) gene expression suggest that both genes may contribute to plaque stability in a coordinated way
Polymorphisms of HDAC9 (show HDAC9 ELISA Kits) is associated with Ischemic Stroke.
This study demonstrated that hdac7 decrease in skeletal muscle in muscle atrophy.
HDAC7 in osteoclasts is an important molecular regulator of MITF (show MITF ELISA Kits) activity and bone homeostasis.
Hdac7 degradation enhances beta-catenin (show CTNNB1 ELISA Kits) transcriptional activity in growth plate chondrocytes.
In hepatic stellate cells, CYLD (show CYLD ELISA Kits) removed HDAC7 from the hepatocyte growth factor (show HGF ELISA Kits) promoter and induced HGF (show HGF ELISA Kits) expression.
Histone deacetylase 7 promotes Toll-like receptor 4 (show TLR4 ELISA Kits)-dependent proinflammatory gene expression in macrophages.
HDAC7 overexpression suppresses, whereas HDAC7 deletion enhances, osteoclastogenesis
Nuclear export of histone deacetylase 7 during thymic selection is required for immune self-tolerance
Splicing of histone deacetylase 7 modulates smooth muscle cell proliferation and neointima formation through nuclear beta-catenin (show CTNNB1 ELISA Kits) translocation.
Data suggest that HDAC7 nuclear export governs a self-sustaining autoexcitatory loop.
Data indicate that CTLs had high expression of the histone deacetylase (show HDAC1 ELISA Kits) HDAC7 but continually phosphorylated and exported this transcriptional repressor from the nucleus.
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 7
, histone deacetylase 7A
, MEF-2 interacting transcription repressor (MITR) protein
, histone deacetylase 4/5-related protein
, histone deacetylase 7B