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Human Monoclonal HDAC2 Primary Antibody for ICC, IF - ABIN2668730
Nayak, Glöckner-Pagel, Vaeth, Schumann, Buttmann, Bopp, Schmitt, Serfling, Berberich-Siebelt: Sumoylation of the transcription factor NFATc1 leads to its subnuclear relocalization and interleukin-2 repression by histone deacetylase. in The Journal of biological chemistry 2009
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Chicken Polyclonal HDAC2 Primary Antibody for ICC, WB - ABIN223296
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
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Human Polyclonal HDAC2 Primary Antibody for IHC (p), WB - ABIN5518663
Chen, Bai, Zhong, Xie, Long, Yang, Wu, Jia, Wang: Wogonin has multiple anti-cancer effects by regulating c-Myc/SKP2/Fbw7? and HDAC1/HDAC2 pathways and inducing apoptosis in human lung adenocarcinoma cell line A549. in PLoS ONE 2013
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Human Monoclonal HDAC2 Primary Antibody for WB - ABIN1882048
Yang, Inouye, Zeng, Bearss, Seto: Transcriptional repression by YY1 is mediated by interaction with a mammalian homolog of the yeast global regulator RPD3. in Proceedings of the National Academy of Sciences of the United States of America 1996
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Human Polyclonal HDAC2 Primary Antibody for WB - ABIN3042622
Chen, Xie, Zhao, Wang, Bai, Yin, Jiang, Xie, Jia, Huang et al.: Ampelopsin induces apoptosis by regulating multiple c?Myc/S?phase kinase?associated protein 2/F?box and WD repeat?containing protein 7/histone deacetylase 2 pathways in human lung adenocarcinoma ... in Molecular medicine reports 2014
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Mouse (Murine) Monoclonal HDAC2 Primary Antibody for ChIP, ICC - ABIN1042602
Zupkovitz, Tischler, Posch, Sadzak, Ramsauer, Egger, Grausenburger, Schweifer, Chiocca, Decker, Seiser: Negative and positive regulation of gene expression by mouse histone deacetylase 1. in Molecular and cellular biology 2006
Human Polyclonal HDAC2 Primary Antibody for IF (p), IHC (p) - ABIN801348
Jou, Chen, Liu, Way, Lai, Hua, Wang, Huang, Kao, Lin: Quantitative phosphoproteomic analysis reveals ?-bisabolene inducing p53-mediated apoptosis of human oral squamous cell carcinoma via HDAC2 inhibition and ERK1/2 activation. in Proteomics 2015
Human Polyclonal HDAC2 Primary Antibody for WB - ABIN966259
Betz, Gray, Ekström, Larsson, Ekström: Human histone deacetylase 2, HDAC2 (Human RPD3), is localized to 6q21 by radiation hybrid mapping. in Genomics 1998
Human Polyclonal HDAC2 Primary Antibody for FACS, IF - ABIN653718
Ishikawa, Miyoshi, Nose, Shibanuma: Transcriptional induction of MMP-10 by TGF-beta, mediated by activation of MEF2A and downregulation of class IIa HDACs. in Oncogene 2010
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Human Polyclonal HDAC2 Primary Antibody for ICC, IF - ABIN4317578
Sirchia, Faversani, Rovina, Russo, Paganini, Savi, Augello, Rosso, Del Gobbo, Tabano, Bosari, Miozzo: Epigenetic effects of chromatin remodeling agents on organotypic cultures. in Epigenomics 2016
HDAC2 seems to be one of the markers of glucocorticosteroid resistance in children with primary nephrotic syndrome
HDAC1,2 inhibitor either alone or when combined with doxorubicin decreases leukemia burden.
Results found that HDAC2 expression is up-regulated in patients with chronic diabetic foot ulcer and in high glucose induced endothelial progenitor cells.
Comparative molecular docking studies of the lead RH01652 with class I HDACs (HDAC1, HDAC2, HDAC3, and HDAC8) shows higher binding affinity towards HDAC2. Thus, lead RH01652 could serve as template to design novel and potent inhibitor of HDAC2.
human immortalized telencephalic/mesencephalic microglial cells reveal significant upregulation of HDAC2 in the presence of the potent microglial activator lipopolysaccharide
the knockdown of HDAC1/2 upregulated KLF5 protein but not KLF5 mRNA, and the increase in KLF5 protein level by silencing HDAC1/2 was at least in part due to decreased proteasomal degradation.
we found that HDAC2 was the direct target of miR-31 by binding to 3'-UTR from the results of luciferase reporter assays, qRT-PCR, and western blotting. HDAC2 played an activation role in tumor growth, whose expression is upregulated and inversely associated with miR-31 levels
data indicate that the obesity impacts on H4ac levels and that strenuous exercise leads to an enhanced chronic low-grade inflammation profile in obesity via an imbalance on H4ac/HDAC2.
Taken together, these data clearly show that FKBP3/Sp1/HDAC2/p27 control cell proliferation during non-small cell lung cancer development.
HDAC1 and HDAC2 suppress the expression of PPP2R3A/PR130, a regulatory subunit of the trimeric serine/threonine phosphatase 2 (PP2A).
Knockdown of HDAC2 completely mimicked the effects of 1,25(OH)2D3 on PTEN gene expression.
Muscle biopsies of chronic obstructive pulmonary disease significantly correlated with HDAC2 decrease compared to controls.
Nuclear HDAC2 immunopositivity was significantly higher in actinic cheilitis (AC) when compared with lip squamous cell carcinoma (LSCC). HDAC1 and HAT1 nuclear immunostaining were higher in AC, with no statistical significance. When comparing data with our previous study, we found a positive correlation between HDAC1 X DNMT1/DNMT3b, HDAC2 X DNMT3b, and HAT1 X DNMT1/DNMT3b for certain studied groups.
With tissue microarrays of hepatocellular carcinoma (HCC) patients, we determined the prognostic values of the core genes in the network and found that RAD21, CDK1, and HDAC2 expression levels were negatively associated with overall survival for HCC patients.
Histone deacetylases 1 and 2 cooperate in regulating BRCA1, CHK1, and RAD51 expression in acute myeloid leukemia cells.
Combined treatment with the histone deacetylase inhibitors (HDACi) suberoylanilide hydroxamic acid plus 5-fluorouracil (5-FU) and oxaliplatin (Oxa) reduced the level of HDAC2 expression in HT-29 cells.
miR-223 controls the expression of CX3CL1 by targeting HDAC2 in chronic obstructive pulmonary disease patients and mouse models of the disease.
Data show that BRCA2 was required for HDAC2/3 association with acetylated BubR1 in nocodazole (Noc)-arrested cells.
study defines two classes of HDAC2 targets in human cells, with a dependence of HDAC1 on HDAC2 at one class of targets, and distinguishes unique functions for HDAC2
This study demonstrated that the Expression of HDAC2 Transcript Is Reduced in Dorsolateral Prefrontal Cortex of Patients with Schizophrenia.
The results suggest that the interaction between Zeb1, Hdac2, and eNOS is required for early mesendodermal differentiation of naive mouse embryonic stem cells.
Hdac1 and Hdac2 as regulators of microglia activation, proliferation, and phagocytosis that define microglia features during the specific conditions of prenatal development and AD-associated neurodegeneration. In contrast, we found that deficiency of Hdac1 and Hdac2 in neuroectodermal cells was not able to modulate amyloid plaque formation.
An early response to nerve injury has been identified that controlled by HDAC2, which coordinates the action of other chromatin remodeling enzymes to induce the upregulation of Oct6, a key transcription factor for Schwann cells development.
The activity of HDAC2 and HDAC8 was elevated 7 days after the ischemia both in neurons and astrocytes of the studied brain structures.
these data demonstrate the preclinical efficacy of targeting the downstream HDAC1/2-Gli1 acetylation in the treatment of SHH Medulloblastoma.
miR-455-3p activated Nrf2/ARE signal pathway through suppressing Keap1 via negative regulating HDAC2 protein level, thereby suppressing oxidative stress and promoting osteoblasts growth.
results show that Hdac1 and Hdac2 function redundantly within the neural crest to regulate proliferation and the development of the pharyngeal arches by means of repression of cyclin-dependent kinase inhibitors.
The E26 transformation-specific transcription factor, ETV4, which is induced by fibroblast growth factor signalling and acts as a repressor of ZRS activity, interacts with the histone deacetylase HDAC2 and ensures that the poised ZRS remains transcriptionally inactive.
In the delayed phase after stroke, administration of HDAC2 inhibitors promoted functional recovery via epigenetically increased neuroplasticity-related genes expression leading to circuit reorganization in the peri-infarct area.
Hdac2 silencing in pregnant mice elevated placental P-gp expression and decreased digoxin transplacental transfer rate.
the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.
these findings suggested that HDAC2 may be an important negative regulator involved in chronic stressinduced cognitive impairment.
Study demonstrated that in the mouse liver, HDAC2 is primarily expressed in hepatocytes. CD36 deletion inhibited nuclear expression of HDAC2 in hepatocytes but had no impact on the expression of HDAC2 in macrophages.
Members of the SIN3A/HDAC2 corepressor complex are enriched in an extended NANOG interactome.
The findings suggest that miR-455-3p plays a critical role during chondrogenesis by directly targeting HDAC2/8 and promoting histone H3 acetylation.
Treatment of the haplotype Npr1(+/-) mice with histone deacetylase inhibitors significantly lowered blood pressure and reduced the renal inflammation and fibrosis involving the interactive roles of HDAC1/2, NF-kappaB (p65), and STAT1.
Acetylation-dependent control of global poly(A) RNA degradation by CBP/p300 and HDAC1-HDAC2 has been described.
Our study indicates that ischemia-induced histone deacetylase 2 upregulation from 5 to 7 d after stroke mediates the secondary functional loss by reducing survival and neuroplasticity of peri-infarct neurons as well as augmenting neuroinflammation. Thus, precisely targeting histone deacetylase 2 in the window phase provides a novel therapeutic strategy for stroke recovery.
Taken together, Fam60a is an essential core subunit of a variant Sin3a-Hdac complex in embryonic stem cells that is required to promote rapid proliferation and prevent unscheduled differentiation.
This gene product belongs to the histone deacetylase family. Histone deacetylases act via the formation of large multiprotein complexes, and are responsible for the deacetylation of lysine residues at the N-terminal regions of core histones (H2A, H2B, H3 and H4). This protein forms transcriptional repressor complexes by associating with many different proteins, including YY1, a mammalian zinc-finger transcription factor. Thus, it plays an important role in transcriptional regulation, cell cycle progression and developmental events. Alternative splicing results in multiple transcript variants.
YY1-associated factor 1
, transcriptional regulator homolog RPD3
, YY1 transcription factor-binding protein
, histone deacetylase-2