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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.
Findings provide physiological insight into the ciliary role of the CYLD (show CYLD Proteins)/HDAC6 (show HDAC6 Proteins) axis and suggest a functional interplay between these two proteins in ciliary homeostasis.
Suppression of HDAC6 (show HDAC6 Proteins) enhanced the interaction between HIF-1alpha (show HIF1A Proteins) and HSP70 (show HSP70 Proteins) under hypoxic conditions.
Overall, our results provide the first evidence that HDAC6 (show HDAC6 Proteins) is capable of inducing expression of pro-inflammatory genes by regulating the ROS (show ROS1 Proteins)-MAPK (show MAPK1 Proteins)-NF-kappaB (show NFKB1 Proteins)/AP-1 (show JUN Proteins) pathways and serves as a molecular target for inflammation.
MAP3K4 (show MAP3K4 Proteins) activity controls epithelial-to-mesenchymal transition through the ubiquitination and degradation of HDAC6 (show HDAC6 Proteins).
HDAC6 (show HDAC6 Proteins) is a critical regulator of a pro-apoptotic p53 (show TP53 Proteins) K120 acetylation and mitochondrial function in mesenchymal stem cells
class IIa HDAC (show HDAC3 Proteins) function could be used to enhance metabolic health in chronic diseases driven by physical inactivity.
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.
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
Proper heart valve formation in zebrafish critically depends on protein kinase D2 (show PKD2 Proteins)-histone deacetylase 5-Kruppel-like factor signaling.
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 4
, histone deacetylase mHDA1
, histone deacetylase 5
, histone deacetylase mHDA2
, scurfy candidate 6