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Human Polyclonal HDAC5 Primary Antibody für 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 ... in Molecular and cellular biology 2007
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Human Polyclonal HDAC5 Primary Antibody für 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. in The Journal of biological chemistry 2006
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Human Polyclonal HDAC5 Primary Antibody für IP, IHC - ABIN223300
Yamaguchi, Chakraborty, Pasek, Molkentin, Meissner: Dysfunctional ryanodine receptor and cardiac hypertrophy: role of signaling molecules. in American journal of physiology. Heart and circulatory physiology 2011
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Human Polyclonal HDAC5 Primary Antibody für IHC, WB - ABIN362746
Döppler, Storz, Li, Comb, Toker: A phosphorylation state-specific antibody recognizes Hsp27, a novel substrate of protein kinase D. in The Journal of biological chemistry 2005
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Human Polyclonal HDAC5 Primary Antibody für IHC - ABIN966266
McKinsey, Zhang, Lu, Olson: Signal-dependent nuclear export of a histone deacetylase regulates muscle differentiation. in Nature 2000
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Human Polyclonal HDAC5 Primary Antibody für 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. in Anticancer research 2016
Human Polyclonal HDAC5 Primary Antibody für 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. in Molecular and cellular biology 2005
These results demonstrate a previously unknown negative epigenetic regulation of hematopoietic stem cells (HSC) homing and engraftment by HDAC5, and allow for a new and simple translational strategy to enhance HSC transplantation.
Collectively, these data indicate that vIRF3 alters global gene expression and induces a hypersprouting formation in an HDAC5-binding-dependent and lymphatic endothelial cell-specific manner, ultimately contributing to Kaposi's sarcoma-associated herpesvirus-associated pathogenesis.
High HDAC5 expression is associated with invasion of lung cancer.
HO-1 plays a key role in protecting tumor cells from apoptosis, in a process that involves Smad7 and HDAC4/5 in apoptosis of B-ALL cells
Hdac5 and Hdac6 expression are required for the adequate expression of Icer and adipocyte function. Altered adipose expression of the two Hdacs in obesity by hypoxia may contribute to the development of metabolic abnormalities.
These findings demonstrate a novel mechanism for deregulation of HDAC5 in non-small cell lung cancer (NSCLC)and suggest that miR5895p/HDAC5 pathway may represent a new prognostic biomarker and therapeutic target against NSCLC.
HDAC5 was extensively expressed in human BC tissues, and high HDAC5 expression was associated with an inferior prognosis.
HDAC5 is a negative predictor of disease-free and overall survival in pancreatic neuroendocrine tumor patients.
Interference with both glucose and glutamine supply in HDAC5-inhibited cancer cells significantly increases apoptotic cell death.
these results suggest that HDAC5 is critical in regulating LSD1 protein stability through post-translational modification, and the HDAC5-LSD1 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) compared to healthy control endothelial cells. Silencing of HDAC5 in SSc ECs restored normal angiogenesis. HDAC5 knockdown followed by ATAC-seq assay in SSc ECs identified key HDAC5-regulated genes involved in angiogenesis and fibrosis, such as CYR61, PVRL2, and FSTL1.
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 in hepatocellular carcinoma cells, which suggested the critical role of histone deacetylase 5-homeodomain-interacting protein kinase-2-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 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 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 transcriptional activation and eNOS expression.
Studied phosphorylation sites within functional HDAC5 domains, including the deacetylation domain (DAC, Ser755), nuclear export signal (NES, Ser1108), and an acidic domain (AD, Ser611).
Exercise-induced GLUT4 transcription via inactivation of HDAC4/5 in mouse skeletal muscle in an AMPKalpha2-dependent manner.
class IIa HDAC function could be used to enhance metabolic health in chronic diseases driven by physical inactivity.
HDAC5 emerges as a cellular conductor of MEF2C and M6a activity and is regulated by miR-124 and miR-9 to control neurite development.
This paper presents data for the first time directly supporting the role of HDAC5 as a scaffold recruiting a chromatin modifying co-repressor complex to specific transcription factors on unique gene promoters. These data for HDAC5 may reflect one of the functions of class IIa HDACs in transcriptional regulation distinct from its catalytic activity.
This study demonstrated that decreased HDAC5 function is able to exacerbate the long-term behavioral effects of adverse rearing environment in mice
As HDAC5 expression may help nullify AIS 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.
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 exon IV resulting in the decreased expression of BDNF.
inhibition of HDAC5 differentially regulates ghrelin and NUCB2/ nesfatin-1 expression by enhancing the acetylation and phosphorylation of Raptor, which subsequently suppress mTORC1 signaling
Results suggest a role for Hdac5 and Sirt2 in neuronal adaptations induced by chronic stress and antidepressant treatment and highlight the therapeutic potential of these targets in the treatment of depression
loss of HDAC5 weakens Treg suppressive function and iTreg formation, as well as IFN-gamma production in CD8+ T cells. Mice lacking HDAC5 do not develop spontaneous illness and do not have enhanced anti-tumor immunity.
increased sclerostin production achieved by HDAC5 shRNA is abrogated by simultaneous knockdown of MEF2C, indicating that MEF2C is a major target of HDAC5 in osteocytes
findings suggest a model in which filamin A local translation following axon injury controls localized HDAC5 activity to promote axon regeneration.
Data indicate that 4-phenylbutyric acid (4-PBA) increases glucose transporter type 4 (GLUT4) expression through a mechanism that involves suppression of the histonedeacetylase 5 (HDAC5) pathway, but without involving endoplasmic reticulum stress.
HDAC5 influences BMAL1 acetylation; interfering with normal expression levels of HDAC5 disrupts circadian rhythms.
In mouse muscle compensatory regulation of HDAC5 transcriptional repressor maintains metabolic integrity.
Study found that axon injury in peripheral sensory neurons elicits a back-propagating calcium wave that invades the soma and causes nuclear export of HDAC5 in a PKCmu-dependent manner. Injury-induced HDAC5 nuclear export enhances histone acetylation to activate a proregenerative gene-expression program.
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-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