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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.
In erythroid cells, pull down experiments identified the presence of a novel complex formed by HDAC5, GATA1, EKLF and pERK which was instead undetectable in cells of the megakaryocytic lineage.
Data reveal a novel role of HDAC5 in modulating the KLF2 (show KLF2 Proteins) transcriptional activation and eNOS (show NOS3 Proteins) expression.
Studied phosphorylation sites within functional HDAC5 domains, including the deacetylation domain (DAC (show AADAC Proteins), Ser755), nuclear export signal (NES (show NES Proteins), Ser1108), and an acidic domain (AD, Ser611).
mRNA and protein levels of HDAC5 were up-regulated in human hepatocellular carcinoma.
HDAC5 promoted the Six1 (show SIX1 Proteins) expression.
As HDAC5 expression may help nullify AIS (show AR Proteins) and identify progenitor cells, the precise delivery of miD2861 may serve as a vehicle for monitoring network remodeling with target specificity and signal sensitivity after drug exposure that identifies brain repair processes in adult animals.
HDAC6 (show HDAC6 Proteins)-mediated autophagy negatively regulates primary cilia length during silibinin treatment and has the potential to serve as a therapeutic target for primary cilia-associated ciliopathies.
HDAC6 (show HDAC6 Proteins) is an effector of the immune cytotoxic response that acts by affecting the dynamics, transport and secretion of lytic granules by cytotoxic T lymphocytes.
This study demonstrated that mice with learned helplessness protocol-induced behavioral despair exhibited higher levels of HDAC5 and HDAC5 binding to the promoter region of BDNF (show BDNF Proteins) exon IV resulting in the decreased expression of BDNF (show BDNF Proteins).
It protects neurons from toxicity of prion (show PRNP Proteins) peptide, and that this protection occurs at through the regulation of the PI3k-Akt (show AKT1 Proteins)-mTOR (show FRAP1 Proteins) axis.
mass spectrometry-based quantitative comparison of acetylated peptides from wild-type vs HDAC6 (show HDAC6 Proteins) knockout mice allowed to identify six new deacetylation sites possibly mediated by HDAC6 (show HDAC6 Proteins).
We therefore tested that reducing HDAC6 (show HDAC6 Proteins) levels by genetic manipulation would attenuate early cognitive and behavioral deficits in R6/1 mice
HDAC6 plays an important role in the function of CMA pathway under the HI stress induced by SCI and it may be a potential therapeutic target in acute SCI model.
inhibition of HDAC5 differentially regulates ghrelin (show GHRL Proteins) and NUCB2/ nesfatin-1 (show NUCB2 Proteins) expression by enhancing the acetylation and phosphorylation of Raptor (show RPTOR Proteins), which subsequently suppress mTORC1 signaling
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