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Human Polyclonal HDAC5 Primary Antibody pour IHC, WB - ABIN362218
Lim, Luo, Koh, Yang, bin Abdul Kadir, Tan, Ye, Wang, Melamed et al.: Distinct mechanisms involving diverse histone deacetylases repress expression of the two gonadotropin beta-subunit genes in immature gonadotropes, and their actions are overcome by ... dans Molecular and cellular biology 2007
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Human Polyclonal HDAC5 Primary Antibody pour ChIP, WB - ABIN2668266
Basile, Mantovani, Imbriano: DNA damage promotes histone deacetylase 4 nuclear localization and repression of G2/M promoters, via p53 C-terminal lysines. dans The Journal of biological chemistry 2006
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Human Polyclonal HDAC5 Primary Antibody pour IHC - ABIN966266
Döppler, Storz, Li, Comb, Toker: A phosphorylation state-specific antibody recognizes Hsp27, a novel substrate of protein kinase D. dans The Journal of biological chemistry 2005
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Human HDAC5 Primary Antibody pour IHC - ABIN966265
McKinsey, Zhang, Lu, Olson: Signal-dependent nuclear export of a histone deacetylase regulates muscle differentiation. dans Nature 2000
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Human Polyclonal HDAC5 Primary Antibody pour IP, IHC - ABIN223300
Yamaguchi, Chakraborty, Pasek, Molkentin, Meissner: Dysfunctional ryanodine receptor and cardiac hypertrophy: role of signaling molecules. dans American journal of physiology. Heart and circulatory physiology 2011
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Human Polyclonal HDAC5 Primary Antibody pour IHC, WB - ABIN362746
Batchvarov, Camm: Prolongation of the QT interval and ventricular arrhythmias: some early observations. dans Heart rhythm : the official journal of the Heart Rhythm Society 2008
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Human Polyclonal HDAC5 Primary Antibody pour ChIP, IP - ABIN4316754
Imbriano, Gurtner, Cocchiarella, Di Agostino, Basile, Gostissa, Dobbelstein, Del Sal, Piaggio, Mantovani: Direct p53 transcriptional repression: in vivo analysis of CCAAT-containing G2/M promoters. dans Molecular and cellular biology 2005
Human Polyclonal HDAC5 Primary Antibody pour ICC, IF - ABIN4316758
Baek, Park, Rhim, Park, Kim, Kim, Nam: Immunohistochemical Characterization of Histone Deacetylase as a Potential Prognostic Marker and Therapeutic Target in Endometrial Stromal Sarcoma. dans Anticancer research 2016
HDAC5 is a negative predictor of disease-free and overall survival in pancreatic neuroendocrine tumor patients.
Interference with both glucose and glutamine (Montrer GFPT1 Anticorps) supply in HDAC5-inhibited cancer cells significantly increases apoptotic cell death.
these results suggest that HDAC5 is critical in regulating LSD1 (Montrer KDM1A Anticorps) protein stability through post-translational modification, and the HDAC5-LSD1 (Montrer KDM1A Anticorps) 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 (Montrer CYP11A1 Anticorps)) compared to healthy control endothelial cells. Silencing of HDAC5 in SSc (Montrer CYP11A1 Anticorps) ECs restored normal angiogenesis. HDAC5 knockdown followed by ATAC (Montrer XCL1 Anticorps)-seq assay in SSc (Montrer CYP11A1 Anticorps) ECs identified key HDAC5-regulated genes involved in angiogenesis and fibrosis, such as CYR61 (Montrer CYR61 Anticorps), PVRL2 (Montrer PVRL2 Anticorps), and FSTL1 (Montrer FSTL1 Anticorps).
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 (Montrer HIPK2 Anticorps) in hepatocellular carcinoma cells, which suggested the critical role of histone deacetylase 5-homeodomain-interacting protein kinase-2 (Montrer HIPK2 Anticorps)-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 (Montrer HDAC6 Anticorps) 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 (Montrer ITK Anticorps) through inhibition of HDAC5.
These results suggest a strong regulatory function of HDAC5 in the pro-inflammatory response of macrophages.
HDAC6 (Montrer HDAC6 Anticorps) inhibition reduces cell growth primarily by reducing intracellular cAMP and Ca(2 (Montrer CA2 Anticorps)+) levels.
These data thus reveal that HDAC6 (Montrer HDAC6 Anticorps) represses IL-17 (Montrer IL17A Anticorps) production in T cells, providing novel insights into the role of HDAC6 (Montrer HDAC6 Anticorps) in the immune system.
A decrease of HDAC6 (Montrer HDAC6 Anticorps) expression caused by Helicobacter pylori infection is associated with oncogenic transformation in gastric cancer.
HDAC5 emerges as a cellular conductor of MEF2C (Montrer MEF2C Anticorps) and M6a (Montrer GPM6A Anticorps) activity and is regulated by miR (Montrer MLXIP Anticorps)-124 and miR (Montrer MLXIP Anticorps)-9 to control neurite development.
HDAC6 (Montrer HDAC6 Anticorps) inhibition reduces tumor growth and PD-L1 (Montrer CD274 Anticorps) production in vivo.
Specific HDAC6 (Montrer HDAC6 Anticorps) inhibitor, tubacin, reduced cyst growth by inhibiting proliferation of cyst-lining epithelial cells, downregulated cyclic AMP (Montrer TMPRSS5 Anticorps) levels, and improved renal function in mouse model of autosomal dominant polycystic kidney disease (ADPKD). Thus, HDAC6 (Montrer HDAC6 Anticorps) 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 (Montrer HDAC6 Anticorps) protein).
ARID1A (Montrer ARID1A Anticorps) mutation inactivates the apoptosis-promoting function of p53 (Montrer TP53 Anticorps) by upregulating HDAC6 (Montrer HDAC6 Anticorps), indicating that pharmacological inhibition of HDAC6 (Montrer HDAC6 Anticorps) is a therapeutic strategy for ARID1A (Montrer ARID1A Anticorps)-mutated cancers.
Fatty acids prevent CIDEC (Montrer CIDEC Anticorps) deacetylation by promoting the dissociation of CIDEC (Montrer CIDEC Anticorps) from HDAC6 (Montrer HDAC6 Anticorps), resultin in increased association of CIDEC (Montrer CIDEC Anticorps) with PCAF (Montrer KAT2B Anticorps) 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