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HDAC5 is a negative predictor of disease-free and overall survival in pancreatic neuroendocrine tumor patients.
Interference with both glucose and glutamine (show GFPT1 Proteins) supply in HDAC5-inhibited cancer cells significantly increases apoptotic cell death.
these results suggest that HDAC5 is critical in regulating LSD1 (show KDM1A Proteins) protein stability through post-translational modification, and the HDAC5-LSD1 (show KDM1A Proteins) axis has an important role in promoting breast cancer development and progression.
The expression of HDAC5 was significantly increased in endothelial cells (ECs) from patients with systemic sclerosis (SSc (show CYP11A1 Proteins)) compared to healthy control endothelial cells. Silencing of HDAC5 in SSc (show CYP11A1 Proteins) ECs restored normal angiogenesis. HDAC5 knockdown followed by ATAC (show XCL1 Proteins)-seq assay in SSc (show CYP11A1 Proteins) ECs identified key HDAC5-regulated genes involved in angiogenesis and fibrosis, such as CYR61 (show CYR61 Proteins), PVRL2 (show PVRL2 Proteins), and FSTL1 (show FSTL1 Proteins).
the migration and invasion of hepatocellular carcinoma cells were impaired by knockdown of histone deacetylase 5 or hypoxia-inducible factor-1alpha but rescued when eliminating homeodomain-interacting protein kinase-2 (show HIPK2 Proteins) in hepatocellular carcinoma cells, which suggested the critical role of histone deacetylase 5-homeodomain-interacting protein kinase-2 (show HIPK2 Proteins)-hypoxia-inducible factor-1alpha pathway in hypoxia-induced metastasis.
HDAC5 inhibits hepatic lipogenic genes expression by attenuating the transcriptional activity of liver X receptor.
HDAC5 promotes cellular proliferation through the upregulation of cMet, and may provide a novel therapeutic target for the treatment of patients with Wilms' tumor.
HDAC5 and HDAC6 (show HDAC6 Proteins) were highly expressed in melanoma cells but exhibited low expression levels in normal skin cells.
Formononetin-combined therapy may enhance the therapeutic efficacy of doxorubicin in glioma cells by preventing EMT (show ITK Proteins) through inhibition of HDAC5.
These results suggest a strong regulatory function of HDAC5 in the pro-inflammatory response of macrophages.
HDAC6 (show HDAC6 Proteins) inhibition reduces cell growth primarily by reducing intracellular cAMP and Ca(2 (show CA2 Proteins)+) levels.
These data thus reveal that HDAC6 (show HDAC6 Proteins) represses IL-17 (show IL17A Proteins) production in T cells, providing novel insights into the role of HDAC6 (show HDAC6 Proteins) in the immune system.
A decrease of HDAC6 (show HDAC6 Proteins) expression caused by Helicobacter pylori infection is associated with oncogenic transformation in gastric cancer.
HDAC5 emerges as a cellular conductor of MEF2C (show MEF2C Proteins) and M6a (show GPM6A Proteins) activity and is regulated by miR (show MLXIP Proteins)-124 and miR (show MLXIP Proteins)-9 to control neurite development.
HDAC6 (show HDAC6 Proteins) inhibition reduces tumor growth and PD-L1 (show CD274 Proteins) production in vivo.
Specific HDAC6 (show HDAC6 Proteins) inhibitor, tubacin, reduced cyst growth by inhibiting proliferation of cyst-lining epithelial cells, downregulated cyclic AMP (show TMPRSS5 Proteins) levels, and improved renal function in mouse model of autosomal dominant polycystic kidney disease (ADPKD). Thus, HDAC6 (show HDAC6 Proteins) could play a role in cyst formation and could serve as a potential therapeutic target in ADPKD.
Data suggest that a switch in post-translational processing of Tau from acetylation at Lys321 to phosphorylation at Ser324 coordinately regulates Tau aggregation and may be relevant in tauopathy and Alzheimer disease; acetylation/phosphorylation of Tau appears to be controlled by Hdac6 (histone deacetylase 6 (show HDAC6 Proteins) protein).
ARID1A mutation inactivates the apoptosis-promoting function of p53 by upregulating HDAC6, indicating that pharmacological inhibition of HDAC6 is a therapeutic strategy for ARID1A-mutated cancers.
Fatty acids prevent CIDEC (show CIDEC Proteins) deacetylation by promoting the dissociation of CIDEC (show CIDEC Proteins) from HDAC6 (show HDAC6 Proteins), resultin in increased association of CIDEC (show CIDEC Proteins) with PCAF (show KAT2B Proteins) on the endoplasmic reticulum.
findings showed that CAMDI regulates neuronal migration through the modulation of HDAC6 and indicate that HDAC6 hyperactivation by CAMDI deletion causes psychiatric behaviors, at least in part, through delayed radial migration due to impaired centrosomes
Protein kinase D-HDAC5 pathway plays an important role in VEGF regulation of gene transcription and angiogenesis
Regulation of flowering time by the histone deacetylase HDA5
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 belongs to the class II histone deacetylase/acuc/apha family. It possesses histone deacetylase activity and represses transcription when tethered to a promoter. It coimmunoprecipitates only with HDAC3 family member and might form multicomplex proteins. It also interacts with myocyte enhancer factor-2 (MEF2) proteins, resulting in repression of MEF2-dependent genes. This gene is thought to be associated with colon cancer. Two transcript variants encoding different isoforms have been found for this gene.
histone deacetylase 5
, antigen NY-CO-9
, histone deacetylase 4
, histone deacetylase mHDA1
, histone deacetylase mHDA2
, scurfy candidate 6