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Human Polyclonal HDAC8 Primary Antibody for IHC (p), ELISA - ABIN543298
Hu, Chen, Fredrickson, Zhu, Kirkpatrick, Zhang, Johanson, Sung, Liu, Winkler: Cloning and characterization of a novel human class I histone deacetylase that functions as a transcription repressor. in The Journal of biological chemistry 2000
Show all 3 Pubmed References
Human Polyclonal HDAC8 Primary Antibody for ICC, IF - ABIN4317610
Emmons, Faião-Flores, Sharma, Thapa, Messina, Becker, Schadendorf, Seto, Sondak, Koomen, Chen, Lau, Wan, Licht, Smalley: HDAC8 Regulates a Stress Response Pathway in Melanoma to Mediate Escape from BRAF Inhibitor Therapy. in Cancer research 2019
Human Polyclonal HDAC8 Primary Antibody for IP, IHC - ABIN223303
Mao, Hou, Cao, Wang, Li, Chen, Fei, Hurren, Gronda, Wu, Trudel, Schimmer: The tricyclic antidepressant amitriptyline inhibits D-cyclin transactivation and induces myeloma cell apoptosis by inhibiting histone deacetylases: in vitro and in silico evidence. in Molecular pharmacology 2011
Human Polyclonal HDAC8 Primary Antibody for IHC - ABIN966268
Lee, Rezai-Zadeh, Seto: Negative regulation of histone deacetylase 8 activity by cyclic AMP-dependent protein kinase A. in Molecular and cellular biology 2003
AC-miR-95-5p-Exos may act as an HDAC2/8 inhibitor and exhibit potential as a disease-modifying osteoarthritis drug.
High HDAC8 expression is associated with breast cancer.
These data suggest that HDAC8 contributes to pulmonary fibrosis and that there is a therapeutic potential for HDAC8 inhibitors to treat IPF as well as other fibrotic lung diseases.
HDAC8 inhibits cytotoxicity induced by cobalt and hypoxia/reoxygenation, in part, through suppressing DRP1 expression and mitochondrial fission.
HDAC8 enhances the in vitro migration abilities of breast cancer cells, stabilizes the expression and increases the nuclear localization of Yes-associated protein (YAP).
Knockdown of HDAC8 by siRNA, inhibition of HDAC8 and/or HDAC6 by PCI-34051 and tubastatin respectively, cell-migration, cell morphology and cell cycle analysis clearly explained HDAC8 as tubulin deacetylase in HeLa cells and HDAC6 in HEK 293 T cells.
we report a de novo missense HDAC8 mutation that causes overlapping features of Rett-related disorder and Cornelia de Lange syndrome. It is possible that this HDAC8 mutation may be harmful via MECP recruitment, and may consequently cause Rett-related disorder
this study identifies additional underlying causes of CdLS, describes the first instance of a somatic HDAC8 mutation in an individual with CdLS features and provides insight into the molecular bases of HDAC8 deletions.
The present study identified a novel missense mutation (c.806T>G, p.I269R) in the HDAC8 gene leading to Cornelia de Lange Syndrome (CdLS), which not only provided strong evidence for diagnosis in this present patient, but also expanded the spectrum of pathogenic mutations for CdLS.
chemical crosslinking approach identified novel HDAC8-specific substrates with high catalytic efficiency, thus presenting a general strategy for unbiased deacetylase substrate discovery
Co2+ and Zn2+ are the most active metals in HDAC8 biocatalysis, followed by Fe2+, and Mn2+ and Mg2+ to be the least active.
MSC from MPN have higher expression of HDAC8 than normal ones, and the inhibition of HDAC8 expression by its specific inhibitor decreases the capacity of the stroma to support hematopoietic cells from MPN patients, suggesting that HDAC8 may be a potential therapeutic target in this setting.
This study for the first time demonstrated that HDAC8 activity determines susceptibility to cell cycle arrest induced by Anthrax Lethal Toxin, through regulating the PI3K-PTEN-AKT signaling axis.
AHR regulated cell proliferation and tumorigenesis by directly targeting and activating HDAC8 expression in hepatocellular carcinoma cells.
The Epac-Rap1-Akt pathway mediates cAMP signaling-induced inhibition of JNK-dependent HDAC8 degradation, and the resulting HDAC8 increase augments cisplatin-induced apoptosis by repressing TIPRL expression in H1299 lung cancer cells.
The X-ray crystal structure of HDAC8 complexed with inhibitor confirms the formation of a unique subpocket in HDAC8.
These data provide support for the hypothesis that HDAC8 may undergo metal switching in vivo that, in turn, may regulate its activity. However, future studies are needed to explore the identity of the metal ion bound to HDAC8 in cells under varied conditions
The study reports the crystal structure of the HDAC8-trapoxin A complex at 1.24 A resolution, revealing that the ketone moiety of l-Aoe undergoes nucleophilic attack to form a zinc-bound tetrahedral gem-diolate that mimics the tetrahedral intermediate and its flanking transition states in catalysis.
The findings suggest that miR-455-3p plays a critical role during chondrogenesis by directly targeting HDAC2/8 and promoting histone H3 acetylation.
7-amino-4-methylcoumarin did not affect acetyllysine preference in a multiply acetylated substrate. In contrast, AMC significantly enhanced KDAC6 substrate affinity, greatly reduced Sirt1 activity, eliminated the substrate sequence specificity of KDAC4, and had no consistent effect with KDAC8 substrates.
The activity of HDAC2 and HDAC8 was elevated 7 days after the ischemia both in neurons and astrocytes of the studied brain structures.
HDAC8 regulates neural differentiation by exerting control of embryoid body formation.
Results indicate that HDAC8 functions to modulate p53 activity to ensure long-term hematopoietic stem cells (LT-HSCs) maintenance and cell survival under stress.
this study demonstrates a novel role of HDAC8 in LeTx immunotoxicity and regulation of pro-IL-1beta production likely through eRNAs.
HDAC8i induced cell growth inhibition and marked S-phase cell cycle arrest in human and murine-derived MPNST cells
findings show how HDAC8 drives nonalcoholic fatty liver disease-associated hepatocarcinogenesis
Data reveal a role for miR-21-3p in regulating HDAC8 expression and Akt/Gsk3beta pathway in cardiac hypertrophy.
histone deacetylase 8 inhibition reduces gene expression and production of proinflammatory cytokines in vitro and in vivo
HDAC8 and Sirt1 were also demonstrated to interact directly with ERRalpha in vivo and to deacetylate and increase the DNA binding affinity of ERRalpha in vitro.
Global deletion of Hdac8 in mice leads to perinatal lethality due to skull instability, and deletion of Hdac8 in cranial neural crest cells and Hdac8 specifically represses the aberrant expression of homeobox transcription factors such as Otx2 and Lhx1
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 class I of the histone deacetylase family. It catalyzes the deacetylation of lysine residues in the histone N-terminal tails and represses transcription in large multiprotein complexes with transcriptional co-repressors. Multiple transcript variants encoding different isoforms have been found for this gene.
histone deacetylase 8
, histone deacetylase-like 1