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Human Polyclonal HDAC1 Primary Antibody pour IHC, IHC (fro) - ABIN4316727
Wilting, Yanover, Heideman, Jacobs, Horner, van der Torre, DePinho, Dannenberg: Overlapping functions of Hdac1 and Hdac2 in cell cycle regulation and haematopoiesis. dans The EMBO journal 2010
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Human Monoclonal HDAC1 Primary Antibody pour ChIP, ICC - ABIN2668767
Lagger, OCarroll, Rembold, Khier, Tischler, Weitzer, Schuettengruber, Hauser, Brunmeir, Jenuwein, Seiser: Essential function of histone deacetylase 1 in proliferation control and CDK inhibitor repression. dans The EMBO journal 2002
Show all 4 Pubmed References
Human Polyclonal HDAC1 Primary Antibody pour ELISA, WB - ABIN543287
Xia, Anderson, Diaz, Zeleznik-Le: MLL repression domain interacts with histone deacetylases, the polycomb group proteins HPC2 and BMI-1, and the corepressor C-terminal-binding protein. dans Proceedings of the National Academy of Sciences of the United States of America 2003
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Human Polyclonal HDAC1 Primary Antibody pour WB - ABIN550399
Shaw, Zhang, Rzeszutek, Yurkova, Baetz, Davie, Kirshenbaum: Transcriptional silencing of the death gene BNIP3 by cooperative action of NF-kappaB and histone deacetylase 1 in ventricular myocytes. dans Circulation research 2006
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Human Polyclonal HDAC1 Primary Antibody pour IP, IHC - ABIN223295
Cao, Li, Zhu, Shen, Han, Zhang, Yu, Wang, Wu, Chen, Sun, Tang, Zhao, Qiao, Hou, Mao: The antiparasitic clioquinol induces apoptosis in leukemia and myeloma cells by inhibiting histone deacetylase activity. dans The Journal of biological chemistry 2013
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Human Polyclonal HDAC1 Primary Antibody pour WB - ABIN537333
Wilson, Byun, Popova, Murray, LItalien, Sowa, Arango, Velcich, Augenlicht, Mariadason: Histone deacetylase 3 (HDAC3) and other class I HDACs regulate colon cell maturation and p21 expression and are deregulated in human colon cancer. dans The Journal of biological chemistry 2006
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Mouse (Murine) Polyclonal HDAC1 Primary Antibody pour IHC, WB - ABIN3020754
Tao, Hsu, Ma, Cheng, Lee: Epigenetic regulation of HDAC1 SUMOylation as an endogenous neuroprotection against Aβ toxicity in a mouse model of Alzheimer's disease. dans Cell death and differentiation 2018
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Human Polyclonal HDAC1 Primary Antibody pour IHC, WB - ABIN6672064
Zeng, Huang, Wang, Wu, Wu, Huang: Galangin-induced down-regulation of BACE1 by epigenetic mechanisms in SH-SY5Y cells. dans Neuroscience 2015
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Human Polyclonal HDAC1 Primary Antibody pour IHC, ELISA - ABIN129652
Scharer, Barwick, Guo, Bally, Boss: Plasma cell differentiation is controlled by multiple cell division-coupled epigenetic programs. dans Nature communications 2018
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Human Monoclonal HDAC1 Primary Antibody pour IF, IHC (p) - ABIN516392
Nakayama, Mikoshiba, Akagawa: The cell- and tissue-specific transcription mechanism of the TATA-less syntaxin 1A gene. dans FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2016
High HDAC1 expression is associated with Intrahepatic Cholangiocarcinoma.
HDAC1 promotes glycolysis in gastric cancer and affects HIF-1alpha activity in tumor progression and metastasis. HDAC1(High) expression was also an independent adverse prognostic factor for overall survival and disease-free survival
This tag-mediated reprogramming of the HDAC1/2 protein interaction network suggests a mechanism whereby HDAC1 is first loaded into the CCT complex.
Sox6 as a regulator of pancreatic cancer development was shown to interact with the promoter of Twist1, a helix-loop-helix transcription factor involved in the induction of EMT, and to modulate the expression of Twist1 by recruiting HDAC1 to the promoter of the Twist1 gene.
Authors confirmed that high expression of HDAC1 in CLL patients with TP53 mutation, which is closely related to poor prognosis and drug-resistance.
NLK boosts cell proliferation and E2F1 activity and controls the cell cycle switch by releasing HDAC1 from the E2F1 complex, us priming colorectal cancer progression
Combined inhibition of HDAC1/2 and Brd4 resolved the aberrant ISG expression detected in cells derived from patients with two inherited interferonopathies, ISG15 and USP18 deficiencies, defining a novel therapeutic approach to ISG-associated autoimmune diseases.
sing CRISPR/Cas9 genomic editing, we found that HDAC1 and HDAC2 knockout cells significantly induced cell apoptosis, indicating that the regulation of HDAC1 and HDAC2 is extremely important in maintaining K562 cell survival.
Results reveal a prominent role for transcriptional regulator SIN3A (SIN3A) in the transcriptional response to hypoxia, and suggesting a model where modulation of the associated histone deacetylase 1/2 activity, rather than its recruitment, determines the transcriptional output.
miR-34a promotes the apoptosis of HL-60 cells via regulating HDAC1 expression
Colorectal cancer (CRC) patients with HDAC1 positivity was significantly higher in the group with low miR-449a expression compared to that with high expression. The expression of HDAC1, on the contrary, was higher in metastatic liver tumor, supporting the hypothesis that the HDAC1 is an important target gene of miR-449a in clinical settings.
Reptin directly interacted with histone deacetylase 1 (HDAC1) as the critical mechanism driving non-small cell lung cancer (NSCLC) tumour progression. Pharmacological disruption of the Reptin/HDAC1 complex resulted in a substantial decrease in NSCLC cell proliferation and induced significant sensitisation to cisplatin.
The inhibitors remained bound to their respective targets over time of the simulation and the overall potential energy, root-mean-square deviation, root-mean-square fluctuation profiles suggested that the detected compounds may be potential isoform-selective HDAC inhibitors or serve as promising scaffolds for further optimization towards the design of selective inhibitors for cancer therapy.
aldosterone significantly inhibited H3K9 acetylation by upregulating HDAC1 protein expression levels in the renal distal convoluted tubule cells, resulting in its inability to bind to the KL promoter
Using CRISPR/Cas9 to knock out HDAC1 and HDAC2 genes in SW579 cells, we observed that the histone acetylation level and cell cycle arrest were enhanced without any impact on cell growth. Furthermore, HDAC1 and HDAC2 double knockout (KO) cells showed dramatic cell apoptosis activation compared to HDAC1 and HDAC2 individual KO cells.
HDAC1 expression could be regulated and was negatively correlated with miR-761 in CRC. Authors also indicated that the expression of miR-761 was abnormally downregulated in CRC. Transfection with a miR-761 mimic impeded the growth and invasion of CRC cells.
Sp1 or HDAC1 knock down increased GM2-synthase transcription, and butyrate-mediated activation of GM2-synthase mRNA expression in SK-RC-45 cells was accompanied by Sp1 and HDAC1 loss from the +38/+187 region. Taken together, we have identified an epigenetic mechanism for the de-repression of the GM2-synthase gene in RCC.
The downregulation of HDAC1 inhibited cell proliferation, prevented cell migration, decreased cell invasion, reduced tumor angiogenesis and induced cell apoptosis.
The HDAC1 confers immune-resistance, drug-resistance and stem-like phenotype in tumor cells through its catalytic activity.
Leishmania amazonensis induces HDAC1 in infected macrophages, which contribute to parasite survival and is associated to hiporeactive stage found in Leishmania amazonensis infected patients.
Fuss interacts with Rpd3, and downregulation of rpd3 in gustatory neurons phenocopies the loss of Fuss expression. Surprisingly, there is no colocalization of Fuss with phosphorylated Mad in the larval central nervous system, excluding a direct involvement of Fuss in Dpp/BMP signaling.
aken together, these results reveal that inactivation of Rpd3 independently regulates JNK and Yki activities and that both Hippo and JNK signaling pathways contribute to Rpd3 RNAi-induced apoptosis.
Rpd3 accumulates in the nucleolus in the early stage of starvation, upregulates rRNA synthesis, maintains the polysome amount for translation, and finally increases stress tolerance proteins, such as autophagy-related proteins, to acquire starvation stress resistance.
Hdac1/Rpd3 functions together with self-renewal transcriptional repressors to maintain the erm immature intermediate neural progenitors enhancer in an inactive but poised state in neuroblasts.
This study tested the longevity effects of RPD3 on multiple nutrient levels.
Rpd3 deacetylase in the heart plays a significant role in cardiac function and longevity to systemically modulate the fly's response to the environment
the Atro-Rpd3 complex plays a conserved role to function as a Ci(R) corepressor.
Study shows that Fru forms a complex with the transcriptional cofactor Bonus (Bon), which, in turn, recruits either of two chromatin regulators, Histone deacetylase 1 (HDAC1), which masculinizes individual sexually dimorphic neurons, or Heterochromatin protein 1a (HP1a), which demasculinizes them.
The dose of Rpd3 is critical for normal long-term memory.
Work suggests that Drosophila telomere structure is epigenetically regulated by the histone deacetylase Rpd3.
Our study suggests a specific function for the general chromatin remodeling factor Rpd3 in regulating dendrite targeting in neurons, largely through the postmitotic action of the Pros transcription factor.
The SIN3/RPD3 deacetylase complex is essential for G(2) phase cell cycle progression and regulation of SMRTER corepressor levels.
role of Rpd3 deacetylase and caloric restriction in longevity regulation
Consistent with these biochemical and cytological results, Rpd3 mutations enhance the phenotypes of Pcl mutants, further indicating that RPD3 is required for PcG silencing and possibly for PCL function
findings indicate that Rpd3 contributes to Knirps repression activity in vivo
DHDAC1 and -3 have distinct functions in the control of gene expression
Results suggest that atrophin recruits histone deacetylases 1 and 2 and G9a to modify histone H3K9 and to determine cell fates.
ISWI physically interacts with the histone deacetylase activity of the Sin3A/Rpd3 complex.
Huntington's disease in Drosophila model is most readily impacted by inhibition of Rpd3 and Sir2 either individually or in combination.
The finding that Lid antagonizes Rpd3 function provides an explanation for the genetic classification of Lid as a positive transcription regulator.
these findings elucidate a previously uncharacterized role for HDAC activity in establishing the neural crest stem cell state.
Data show that proto-oncogene transcription factor Ets1 regulates neural crest development through histone deacetylase 1 HDAC1) to down-regulate bone morphogenetic protein (BMP) signaling output and reduce id3 protein expression.
Specific knockdown of HDAC1 by a morpholino (HDAC1-MO) decreased the number of BrdU- and BLBP-labeled cells and increased the acetylation level of histone H4 at lysine 12.
Hdac1 regulates differentiation of liver progenitor cells into hepatocytes via Sox9b and differentiation of LPCs into biliary epithelial cells via Cdk8, Fbxw7, and Notch3 in zebrafish with severe hepatocyte loss.
rbbp4 is required for survival of postmitotic precursors, and hdac1 maintains proliferation of the neural stem cell/progenitor pool.
data represent a step towards the comprehension of HDAC1 regulation by its PTM code, with important implications in unravelling its roles both in physiology and pathology
results indicate that HDAC1 plays an important role in otic vesicle formation.
HDAC activity is necessary for control of cell proliferation and migration of posterior lateral line primordium and hair cell differentiation during early stages of its development in zebrafish.
This study reveals distinct functional and temporal requirements for zebrafish hdac1 during neural crest-derived craniofacial and peripheral neuron development.
Hdac1 is required for expression of erm and fgf20a in rhombomeres; Hdac1-dependent expression of these two genes is attenuated in rhombomere boundary regions by Notch signalling activity
HDAC1 is required for pancreatic epithelial proliferation in development and cancer.
Data indicate a novel role for Hdac1 as a positive regulator of gene transcription during development of the vertebrate CNS.
Findings suggest that Mta3-NuRD complex, inclding component HDAC1, is essential for the initiation of primitive hematopoiesis.
hdac1 is an essential component of the transcriptional silencing machinery that supports the formation and subsequent differentiation of neuronal precursors.
hdac1 is required for the normal formation of craniofacial cartilage and pectoral fins.
in vivo role of HDAC1 in regulating cell cycle progression is region-specific, as HDAC1 promotes cell cycle exit in the retina
Hdac1 antagonizes Wnt and notch signaling pathways to promote cell-cycle exit and subsequent neurogenesis in zebrafish retina
essential component of the mechanism that allocates neural progenitors to the oligodendrocyte fate
Activates non-canonical Wnt signaling underlying axial extension and promotes Wnt-independent caudal migration of a subset of hindbrain branchiomotor neurons in a zebrafish mutant planar cell polarity pathway.
colgate/hdac1 repression of foxd3 expression is required to permit mitfa-dependent melanogenesis.
Hdac1 is crucial for regulating distinct steps in endodermal organogenesis.
Transcription of the HDAC1 gene was repressed by CCAAT/enhancer binding proteins during myeloid differentiation, and activated by GATA-1 during erythro-megakaryocytic differentiation
The effect of p53 expression on the development of cloned embryos, and its interaction with HDAC1 and DNMT3A are reported.
The results suggest that HDAC1 knock-down in oocytes did not influence the rates of maturation or cleavage of parthenogenetic embryos.
Our results uncover a regulatory mechanism in which HDAC1 negatively regulates RBPJ binding on mitotic chromatin in a KDM5A-dependent manner. We propose that relative chromatin affinity of a minimal regulatory complex, reflecting a specific transcription program, renders selective RBPJ binding on mitotic chromatin.
HDAC1 and HDAC2 regulate the spatial positioning of intermediate progenitors to form the subventricular zone. Developmental stage-specific depletion of both HDAC1 and HDAC2 in radial glial progenitors results in mispositioning of IPs at the ventricular surface, where they divide and differentiate into neurons, thereby leading to the cortical malformation.
Our data collectively indicate a role for TLR4-mediated autophagy in cardiac remodeling and contractile dysfunction in aging through a HDAC1-NCoR1-dependent mechanism.
findings uncovered HDAC1 as a novel hepcidin suppressor through complexing with SMAD4 but not deacetylation of either histone 3 or SMAD4; in addition, our study suggested a novel implication of entinostat in treating iron-overload disorders
HDAC1 and HDAC2 modulate TGF-beta signaling
these data demonstrate a novel pathophysiological role for HDAC1 in experimental autoimmune encephalomyelitis
HDAC1 sumoylation plays a dual role in MyoD signaling during myogenesis.
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.
HDAC1 depletion caused early beating of cardiomyocytes compared with those of the wild-type (wt) counterpart.
these data demonstrate the preclinical efficacy of targeting the downstream HDAC1/2-Gli1 acetylation in the treatment of SHH Medulloblastoma.
p75NTR intracellular domain as a retrograde degenerative signal and reveal p150(Glued) deacetylation as a unique mechanism regulating axonal transport
the present study demonstrates that lovastatin inhibits the expression of pro-inflammatory mediators, including iNOS and TNF-alpha, through the suppression of HDAC1 expression, PI3K/Akt phosphorylation and NF-kappaB translocation in LPS-stimulated RAW264.7 macrophage cells.
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 epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.
These data suggest that HDAC1-related H3K9ac plays a key role in Hcy-mediated lipid metabolism disorders, and that miR-34a may be a novel therapeutic target in Hcy-related atherosclerosis.
Early life stress (ELS)-induced schizophrenia-like phenotypes correlate with a widespread increase of Hdac1 expression that is linked to altered DNA methylation. Hdac1 overexpression in neurons of the medial prefrontal cortex, but not in the dorsal or ventral hippocampus, mimics schizophrenia-like phenotypes induced by ELS.
e results showed mTet1 modified mGSCs had better self-renewal and proliferation ability than wild-type mGSCs, mTet1 could also up-regulate JMJD3 to decrease H3K27me3, which also showed to suppress the MEK-ERK pathway. Furthermore, Co-IP analysis demonstrated that TET1 interact with PCNA and HDAC1 by forming protein complexes to comprehensively regulate dairy goat mGSCs and spermatogenesis.
reduced HDAC1 levels at promotors of distinct plasticity-associated genes predispose animals exposed to early life stress to enhanced expression of these genes upon cognitive challenge
HDAC1 SUMOylation functions as an endogenous defense mechanism protecting against Abeta-toxicity. Stimuli such as BDNF, IGF-1 and CRF that increase the level of HDAC1 SUMOylation without altering the HDAC1 expression level
This work therefore identifies a new role for FD in reproductive patterning, as FD regulates IM function together with HDA19 in an age-dependent fashion.
These results reveal the presence of an MSI1-HDA19 complex that fine-tunes abscissic acid signaling in Arabidopsis.
SCL15 acts as an HDA19-associated regulator to repress embryonic traits in seedlings.
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.
HDA19 and HSL1 may act together to repress seed maturation gene expression during germination. HDA19 and HSL1 may play a vital role during embryogenesis.
findings show that AP2 represses its target genes by physically recruiting the co-repressor TOPLESS and the histone deacetylase HDA19
HDA19 plays a negative role in basal defense mediated by the salicylic acid-dependent signaling pathway.
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.[HDA19]
HDA19 may regulate gene expression involved in jasmonic acid and ethylene signaling of pathogen response in Arabidopsis.[HDA19]
Data suggest that AtHD1 is a nuclear protein and possesses histone deacetylase activities responsible for global transcriptional regulation important to plant growth and development.
These results suggest that acetylation of specific histone Lys residues, regulated by GCN5, TAF1, and HD1, is required for light-regulated gene expression.
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.
Disruption of HDA19 leads to compromised resistance, whereas its overexpression results in enhanced resistance to P. syringae.
We further show that G1 arrest is necessary for the histone deacetylase HDA-1, a key regulator of differentiation, to promote pro-invasive gene expression and invadopodia formation.
hda-1 target genes revealed that fos-1 acts downstream of hda-1 in vulval cells, whereas egl-43 and nhr-67 mediate hda-1 function in the gonadal anchor cell.
HDAC behaves as a co-repressor modulating FOS-1-mediated transcriptional regulation
Theses studies define a new role for HDA-1 in nervous system development, and provide the first evidence for HDAC function in regulating neuronal axon guidance.
Data show that the expression levels of the 5 epigenetic modifying genes Dnmt1, Dnmt3a, Hdac1, Kdm3a and Uhrf1 were higher in group pig in highland (TH) than in group Yorkshire in highland (YH).
Histone acetylation and deacetylation, catalyzed by multisubunit complexes, play a key role in the regulation of eukaryotic gene expression. The protein encoded by this gene belongs to the histone deacetylase/acuc/apha family and is a component of the histone deacetylase complex. It also interacts with retinoblastoma tumor-suppressor protein and this complex is a key element in the control of cell proliferation and differentiation. Together with metastasis-associated protein-2, it deacetylates p53 and modulates its effect on cell growth and apoptosis.
reduced potassium dependency, yeast homolog-like 1
, Rpd3 histone deacetylase
, histone Deacetylase-1
, histone deacetylase
, histone deacetylase 1
, histone deacetylase 1 (HDAC1)
, reduced potassium dependency 3
, suppressor of variegation 326
, histone deacetylase 1 b
, histone deacetylase 1-B
, Histone DeAcetylase family member (hda-1)
, histone deacetylase 1 a
, maternally-expressed histone deacetylase
, probable histone deacetylase 1-A
, yeast RPD3 homologue