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Human Polyclonal HDAC6 Primary Antibody for ChIP, WB - ABIN2668292
Ying, Zhang, Zhou, Qu, Wang, Liu, Lu, Zhu: Selective histonedeacetylase inhibitor M344 intervenes in HIV-1 latency through increasing histone acetylation and activation of NF-kappaB. in PLoS ONE 2012
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Human Polyclonal HDAC6 Primary Antibody for IHC, WB - ABIN223301
Wang, Nguyen, McLaughlin, Sikkink, Ramirez-Alvarado, Weinshilboum: Human thiopurine S-methyltransferase pharmacogenetics: variant allozyme misfolding and aggresome formation. in Proceedings of the National Academy of Sciences of the United States of America 2005
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Human Polyclonal HDAC6 Primary Antibody for IF, IHC - ABIN6711785
Chen, Zang, Pan, Zhu, Chen, Chen, Xu: Expression patterns of histone deacetylases in experimental stroke and potential targets for neuroprotection. in Clinical and experimental pharmacology & physiology 2013
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Human Polyclonal HDAC6 Primary Antibody for ELISA - ABIN564313
Xargay-Torrent, López-Guerra, Saborit-Villarroya, Rosich, Campo, Roué, Colomer: Vorinostat-induced apoptosis in mantle cell lymphoma is mediated by acetylation of proapoptotic BH3-only gene promoters. in Clinical cancer research : an official journal of the American Association for Cancer Research 2011
Human Monoclonal HDAC6 Primary Antibody for ELISA, WB - ABIN564314
Bantscheff, Hopf, Savitski, Dittmann, Grandi, Michon, Schlegl, Abraham, Becher, Bergamini, Boesche, Delling, Dümpelfeld, Eberhard, Huthmacher, Mathieson, Poeckel, Reader, Strunk, Sweetman, Kruse et al.: Chemoproteomics profiling of HDAC inhibitors reveals selective targeting of HDAC complexes. ... in Nature biotechnology 2011
Human Polyclonal HDAC6 Primary Antibody for ChIP, IP - ABIN537336
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
Human Polyclonal HDAC6 Primary Antibody for IHC (p), ELISA - ABIN542734
Grozinger, Hassig, Schreiber: Three proteins define a class of human histone deacetylases related to yeast Hda1p. in Proceedings of the National Academy of Sciences of the United States of America 1999
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Human Monoclonal HDAC6 Primary Antibody for FACS, ICC - ABIN4316769
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
Both SQSTM1-HDAC6-dependent autophagy and the aggresome pathway mediate CDK1 degradation in human breast cancer cells.
Which can be reverted by treatment with selective inhibitors of HDAC6.
Increased HDAC6 expression is associated with progression of primary open-angle glaucoma.
HDAC6 expression is regulated by hnRNPK.HDAC6 role in autophagy.
These results connect HDAC6 activity to regulation of total and surface Notch3 levels.
our findings indicated that fibroblastic HDAC6 was a vital epigenetic mediator involved in programming an immunosuppressive tumor microenvironment that dampens antitumor immunity in breast cancer
ERK1 and -2 are acetylated and that HDAC6 promotes ERK1 activity via deacetylation.
These findings highlight an important role of miR-27b in the development of DLBCL and uncover a HDAC6-Rel A/p65-miR-27b-MET signaling pathway. Elevating miR-27b through HDAC6 inhibition would be a promising strategy for DLBCL treatment.
Thus, favorable binding entropy contributes to HDAC6 selectivity. Notably, cyclohexenyl hydroxamate 2 represents a promising lead for derivatization with capping groups that may further enhance its impressive 313-fold thermodynamic selectivity for HDAC6 inhibition.
Histone deacetylase 6 regulated expression of IL-8 is involved in the doxorubicin (Dox) resistance of osteosarcoma cells via modulating ABCB1 transcription
our results identify HDAC6 as a druggable regulator of PAH-PASMC resistance to apoptosis and offer novel insights into the molecular mechanisms governing vascular remodeling.
In this review, we describe the HDACs, their inhibitors, and the recent advances of HDAC6 inhibitors, their mechanisms of action and role in lymphoproliferative disorders.
Mycobacterium tuberculosis infection disturbs the HDAC6/HDAC11 levels to induce IL-10 expression in macrophages.
Histone deacetylase 6 (HDAC6) inhibition enhanced glioma stem cells (GSCs) radiosensitivity via inactivating sonic hedgehog protein (SHH)/glioma-associated oncogene homolog 1 (Gli1) pathway.
Cortactin (CTTN) silencing in megakaryocyte (MK) phenocopies histone deacetylase 6 (HDAC6) inactivation and knockdown leads to a strong proplatelet formation (PPF) defect.
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.
this study reports that HDAC6 is involved in reactive oxygen species-NF-kappaB signaling pathway related to pro-inflammatory cytokine expression
DTBP represents a promising lead structure for the development of HDAC6 inhibitors, with an improvement in specificity conferred by modification of the cap group. We propose for the first time that the underlying mechanism of the anticancer activity of DTBP is attributed to inhibition of HDAC6 activity.
To the best of our knowledge, this is the first report of an HDAC6 selective inhibitor bearing a hydrazide ZBG. Its capability to passively cross the blood-brain barrier (BBB), as observed through PAMPA assays, and its low cytotoxicity in vitro, suggested its potential for drug development.
we observed an homologous-recombination deficiency (HRD)-associated level of HDAC6 overexpression, which supports a potential role for the effectiveness of HDAC inhibitor treatment in HRD tumors that are characterized by low levels of H4 lysine acetylation.
This study demonstrated that the positive regulatory role of HDAC5 in neuropathic pain may function through SOX10-dependent neuronal activation.
data indicate that histone deacetylase 6 (HDAC6) is one of the essential factors for oocyte maturation and asymmetric division via the HDAC6/mTOR or mDia1 pathway.
HDAC6 promotes T-regulatory cell plasticity
These findings suggested that HDAC6 contributes to mitochondrial thermogenesis in brown adipose tissue by increasing UCP1 expression through cAMP-PKA signaling pathway.
overexpression of Hdac6 extends reproductive lifespan in mice
Hdac6-/- mice display low serum levels of inflammatory cytokine IL-6 and correspondingly an increased survival to a systemic infection with Listeria monocytogenes. The impaired bacterial clearance in the absence of HDAC6 appears to be caused by a defect in autophagy.
deletion or inhibition of the cytoplasmic shuttling factor HDAC6 suppressed neuritic tau bead formation in neurons.
HDAC6 inhibition and the regulation of Prx1 activity may play a significant role in protecting retinal cells and in particular photoreceptors.
Results link the aberrant GlyRS-HDAC6 interaction to Charcot-Marie-Tooth disease type 2D pathology and suggest HDAC6 as an effective therapeutic target.
3T3-L1 cells treated with the siRNA against HDAC6 reduced the autophagy level and enhanced collagen-induced cilia elongation, implying that HDAC6 was involved in mediating autophagy
identified that class II histone deacetylase 6 deacetylates and subsequently activates mDia2.
Study demonstrated that global Hdac6 knock-out mice show dopaminergic abnormalities. The behavioral and pharmacological analysis revealed that Hdac6 gene ablation results in an increased response of postsynaptic D2R.
Findings provide physiological insight into the ciliary role of the CYLD/HDAC6 axis and suggest a functional interplay between these two proteins in ciliary homeostasis.
Suppression of HDAC6 enhanced the interaction between HIF-1alpha and HSP70 under hypoxic conditions.
Overall, our results provide the first evidence that HDAC6 is capable of inducing expression of pro-inflammatory genes by regulating the ROS-MAPK-NF-kappaB/AP-1 pathways and serves as a molecular target for inflammation.
MAP3K4 activity controls epithelial-to-mesenchymal transition through the ubiquitination and degradation of HDAC6.
HDAC6 is a critical regulator of a pro-apoptotic p53 K120 acetylation and mitochondrial function in mesenchymal stem cells
HDAC6 inhibition reduces cell growth primarily by reducing intracellular cAMP and Ca(2+) levels.
that HDAC6 is associated physically with the chaperone protein dHsc4/Hsc70 to maintain the proteostasis of PLIN2
HDAC6 is necessary and sufficient for BRP deacetylation. HDAC6 promotes the formation of larger presynaptic densities.
Atrial fibrillation induces remodeling and loss of contractile function, at least in part through HDAC6 activation and subsequent derailment of alpha-tubulin proteostasis and disruption of the cardiomyocyte microtubule structure.
From a genetic screen, we found that a histone deacetylase 6 (HDAC6) null mutation rescued tau-induced MT defects in both muscles and neurons.
Overexpressing any of HDAC 3, 6, or 11 suppresses CGG repeat-induced neurodegeneration in a Drosophila model of fragile X tremor ataxia syndrome.
Data suggest that alpha-synuclein inclusion formation in the presence of HDAC6 protects dopamine neurons from being damaged by oligomers, which may uncover a common mechanism for synucleinopathies.
findings suggest that it may be possible to intervene in neurodegeneration by augmenting HDAC6 to enhance autophagy
Findings indicate that HDAC6 facilitates degradation of potentially noxious protein substrates, contributing vitally to the neuroprotective role of autophagy.
Results suggest that atrophin recruits histone deacetylases 1 and 2 and G9a to modify histone H3K9 and to determine cell fates.
Study detected evidence that recent strongly positive selection has been acting on a 2.7-kb region in an ancestral African population; this region overlaps with the 3' end of HDAC6, a gene that encodes a newly characterized stress surveillance factor.
In coordination with increased HDAC6 phosphorylation, cigarette smoke extract inhibited Akt and activated glycogen synthase kinase (GSK)-3beta.
the histone deacetylase HDA6 can interact with the histone methyltransferases SUVH4, SUVH5, and SUVH6 (SUVH4/5/6).
HDA6 is a general repressor of pathogen defence response and plays important roles in inhibiting and modulating the expression of pathogen-responsive genes in Arabidopsis.
The hda6 mutant showed a BR-repressed phenotype in the dark and was less sensitive to BR biosynthesis inhibitors. Genetic analysis indicated that HDA6 regulates BR signaling through BIN2. Furthermore, we identified K189 of BIN2 as an acetylated site, which can be deacetylated by HDA6 to influence BIN2 activity
The results suggest that HSI2 recruits MED13 and HDA6 to suppress directly a subset of seed maturation genes post-germination.
HDA6 is a component of the TRB2 complex.
Our results indicate that AtMBD6 is involved in RNA-mediated gene silencing and it binds to RNA binding proteins like AtRPS2C, AtAGO4 and AtNTF2. AtMBD6 also interacts with histone deacetylase AtHDA6 that might have a role in chromatin condensation at the targets of RdDM
HDA6 has at least two clearly separable activities in different genomic regions. In addition, we present an unexpected role for HDA6 in the control of DNA methylation at CG dinucleotides.
Data show that both transcript levels and expression patterns of ENHANCER OF TRIPTYCHON AND CAPRICE1 (ETC1) in the root tip were affected in hda6 mutation.
HDC1 is a ubiquitously expressed nuclear protein that interacts with at least two deacetylases (HDA6 and HDA19), promotes histone deacetylation, and attenuates derepression of genes under water stress.
HDA6 and FLD could act together in a protein complex. Increased levels of histone H3 acetylation and H3K4 trimethylation, indicating functional interplay between histone deacetylase and demethylase through HDA6 and FLD interaction in flowering control.
Taken together, these data indicate that HDA6 is a part of the AS1 repressor complex to regulate the KNOX expression in leaf development.
HD2C functionally associates with HDA6 and regulates gene expression through histone modifications.
HDA6 and MET1 interact directly and act together to silence transposable elements by modulating DNA methylation, histone acetylation, and histone methylation status.
HDA6 and HDA19 may play a redundant role in modulating seed germination and salt stress response, as well as ABA- and salt stress-induced gene expression in Arabidopsis.
HDA6 is required for heterochromatic silencing, and the mutation results in loss of heterochromatic histone modification along with aberrant enrichment for euchromatic modification at HDA6 targets.
HDA6 plays a critical role in regulating cold acclimation process that confers freezing resistance on Arabidopsis.
HDA6-involved histone modifications modulate seed germination and the salt stress response.
reveal a futile cycle of unregulated transcription, siRNA production, and siRNA-directed DNA methylation in the absence of HDA6-mediated histone deacetylation
HDA6 erases histone acetylation as a key step in an epigenetic switch mechanism that silences rRNA genes through concerted histone and DNA modifications.
These results suggest that during germination in Arabidopsis, HDA6 and HDA19 redundantly regulate the repression of embryonic properties directly or indirectly via repression of embryo-specific gene function.
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 II of the histone deacetylase/acuc/apha family. It contains an internal duplication of two catalytic domains which appear to function independently of each other. This protein possesses histone deacetylase activity and represses transcription.
histone deacetylase 5
, histone deacetylase mHDA2
, scurfy candidate 6
, histone deacetylase 6
, histone deacetylase HDA2