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HDAC8 were overexpressed in oral squamous cell carcinoma tissues, mainly localized in the cytoplasm.
Study reveals that HDAC8 can bind and catalyze deacetylation of many acetylated peptides with sequences corresponding to cellular, non-histone proteins, thereby opening a new window to the functional role of HDAC8 in cells.
Findings suggest the therapeutic potential of histone deacetylase 8 histone (HDAC8)inhibition to suppress Notch1 (show NOTCH1 ELISA Kits) signaling in breast cancer.
Data show that histone deacetylase 8 (HDAC8) inhibition led to accumulation of acetylated-SMC3 (show SMC3 ELISA Kits) protein but had no influence on the transcription of estrogen-responsive genes.
study elucidates an HDAC8-mediated p53 (show TP53 ELISA Kits)-inactivating mechanism promoting leukemia stem cells activity
Studies indicate that histone deacetylase 8 protein (HDAC8) aberrantly deacetylates p53 (show TP53 ELISA Kits) protein and promotes leukemia stem cells (LSCs) transformation and maintenance.
Our data exhibited an important role of HDAC8 in promoting gastric cancer tumorigenesis and identify this HDAC8 as a potential therapeutic target for the treatment of gastric cancer.
The H143A and H142A/H143A mutants exhibit activity that is >80000-fold lower than that of wild-type HDAC8; the buried D176N and D176A mutants have significant catalytic effects, with more subtle effects caused by D183N and D183A
cAMP signaling increases HDAC8 protein levels by reducing JNK (show MAPK8 ELISA Kits)-mediated autophagy and ubiquitin-proteasome-dependent degradation of the HDAC8 protein in H1299 lung cancer cells.
Report the preparation and biophysical evaluation of five HDAC8 mutants: P91L, G117E, H180R, D233G, and G304R. Additionally, the double mutants D233G-Y306F and P91L-Y306F were prepared to enable cocrystallization of intact enzyme-substrate complexes.
this study demonstrates a novel role of HDAC8 in LeTx immunotoxicity and regulation of pro-IL-1beta (show IL1B ELISA Kits) production likely through eRNAs.
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 (show SIRT1 ELISA Kits) were also demonstrated to interact directly with ERRalpha (show ESRRA ELISA Kits) in vivo and to deacetylate and increase the DNA binding affinity of ERRalpha (show ESRRA ELISA Kits) 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 (show PRRX1 ELISA Kits) transcription factors such as Otx2 (show OTX2 ELISA Kits) and Lhx1 (show LHX1 ELISA Kits)
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