Search results for "Histone Deacetylase 1"

showing 9 items of 9 documents

HDAC1 and HDAC2 integrate the expression of p53 mutants in pancreatic cancer.

2015

Mutation of p53 is a frequent genetic lesion in pancreatic cancer being an unmet clinical challenge. Mutants of p53 have lost the tumour-suppressive functions of wild type p53. In addition, p53 mutants exert tumour-promoting functions, qualifying them as important therapeutic targets. Here, we show that the class I histone deacetylases HDAC1 and HDAC2 contribute to maintain the expression of p53 mutants in human and genetically defined murine pancreatic cancer cells. Our data reveal that the inhibition of these HDACs with small molecule HDAC inhibitors (HDACi), as well as the specific genetic elimination of HDAC1 and HDAC2, reduce the expression of mutant p53 mRNA and protein levels. We fur…

0301 basic medicineCancer ResearchProteasome Endopeptidase ComplexMutantHistone Deacetylase 2Histone Deacetylase 1Biologymedicine.disease_causeMolecular oncologyProto-Oncogene Proteins c-myc03 medical and health sciencesMicePancreatic cancerGeneticsmedicineAnimalsHumansRNA MessengerPromoter Regions GeneticMolecular BiologyRegulation of gene expressionMice KnockoutMutationWild typeCancerProto-Oncogene Proteins c-mdm2medicine.diseaseGenes p53HDAC13. Good healthGene Expression Regulation NeoplasticHistone Deacetylase InhibitorsPancreatic NeoplasmsDisease Models Animal030104 developmental biologyMutationCancer researchOncogene
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A T cell-specific deletion of HDAC1 protects against experimental autoimmune encephalomyelitis.

2017

Multiple sclerosis (MS) is a human neurodegenerative disease characterized by the invasion of autoreactive T cells from the periphery into the CNS. Application of pan-histone deacetylase inhibitors (HDACi) ameliorates experimental autoimmune encephalomyelitis (EAE), an animal model for MS, suggesting that HDACi might be a potential therapeutic strategy for MS. However, the function of individual HDAC members in the pathogenesis of EAE is not known. In this study we report that mice with a T cell-specific deletion of HDAC1 (using the Cd4-Cre deleter strain; HDAC1-cKO) were completely resistant to EAE despite the ability of HDAC1cKO CD4+ T cells to differentiate into Th17 cells. RNA sequencin…

0301 basic medicineReceptors CCR6Encephalomyelitis Autoimmune ExperimentalMultiple SclerosisReceptors CCR4T cellImmunologyCCR4Histone Deacetylase 1C-C chemokine receptor type 6Biologymedicine.disease_causeAutoimmunity03 medical and health sciencesChemokine receptorMice0302 clinical medicineCell MovementmedicineImmunology and AllergyAnimalsHumansCells CulturedMice KnockoutChimeraMultiple sclerosisExperimental autoimmune encephalomyelitisGene targetingmedicine.diseaseMolecular biologyDisease Models Animal030104 developmental biologymedicine.anatomical_structureSTAT1 Transcription FactorCancer researchTh17 Cells030215 immunologyJournal of autoimmunity
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Histone deacetylase inhibition by suberoylanilide hydroxamic acid: a therapeutic approach to treat human uterine leiomyoma.

2022

Objective To evaluate the effect of inhibition of histone deacetylases (HDACs) by suberoylanilide hydroxamic acid (SAHA) treatment of human uterine leiomyoma primary (HULP) cells in vitro on cell proliferation, cell cycle, extracellular matrix (ECM) formation, and transforming growth factor β3 (TGF-β3) signaling. Design Prospective study comparing uterine leiomyoma (UL) vs. adjacent myometrium (MM) tissue and cells with or without SAHA treatment. Setting Hospital and university laboratories. Patient(s) Women with UL without any hormone treatment. Intervention(s) Myomectomy or hysterectomy surgery in women for leiomyoma disease. Main Outcome Measure(s) HDAC activity was assessed by enzyme-li…

AdultAntineoplastic AgentsHistone Deacetylase 1MMP9Histone Deacetylase 6Histone DeacetylasesCyclin D1Transforming Growth Factor beta3Cell proliferation SAHA ULS-ß3 pathway extracellular matrix uterine leiomyomaTumor Cells CulturedHumansViability assayProspective StudiesCell ProliferationVorinostatbiologyLeiomyomaChemistryCell growthCell CycleObstetrics and GynecologyCell cycleMiddle AgedHDAC3Molecular biologyProliferating cell nuclear antigenExtracellular MatrixGene Expression Regulation NeoplasticHistone Deacetylase InhibitorsReproductive MedicineUterine Neoplasmsbiology.proteinFemaleHistone deacetylaseSignal TransductionFertility and sterility
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Negative transcriptional control of ERBB2 gene by MBP-1 and HDAC1: diagnostic implications in breast cancer

2013

Abstract Background The human ERBB2 gene is frequently amplified in breast tumors, and its high expression is associated with poor prognosis. We previously reported a significant inverse correlation between Myc promoter-binding protein-1 (MBP-1) and ERBB2 expression in primary breast invasive ductal carcinoma (IDC). MBP-1 is a transcriptional repressor of the c-MYC gene that acts by binding to the P2 promoter; only one other direct target of MBP-1, the COX2 gene, has been identified so far. Methods To gain new insights into the functional relationship linking MBP-1 and ERBB2 in breast cancer, we have investigated the effects of MBP-1 expression on endogenous ERBB2 transcript and protein lev…

Cancer ResearchMBP-1/EnolaseReceptor ErbB-2Breast NeoplasmsHistone Deacetylase 1BiologyERBB geneBreast cancerTranscriptional regulationTranscription (biology)Histone DeacetylaseBreast CancermedicineTranscriptional regulationBiomarkers TumorTumor Cells CulturedGeneticsHumansMBP-1ERBB2Promoter Regions Geneticskin and connective tissue diseasesGeneReporter geneCarcinoma Ductal BreastCancerTransfectionGenes erbB-2medicine.diseaseImmunohistochemistryHDAC1Neoplasm ProteinsDNA-Binding ProteinsGene Expression Regulation NeoplasticSettore BIO/18 - GeneticaOncologyCancer researchChromatin immunoprecipitationResearch ArticleBMC Cancer
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pRb2/p130-E2F4/5-HDAC1-SUV39H1-p300 and pRb2/p130-E2F4/5-HDAC1-SUV39H1-DNMT1 multimolecular complexes mediate the transcription of estrogen receptor-…

2003

The estrogen receptor-alpha (ER) plays a crucial role in normal breast development and is also linked to development and progression of mammary carcinoma. The transcriptional repression of ER-alpha gene in breast cancer is an area of active investigation with potential clinical significance. However, the molecular mechanisms that regulate the ER-alpha gene expression are not fully understood. Here we show a new molecular mechanism of ER-alpha gene inactivation mediated by pRb2/p130 in ER-negative breast cancer cells. We investigated in vivo occupancy of ER-alpha promoter by pRb2/p130-E2F4/5-HDAC1-SUV39 H1-p300 and pRb2/p130-E2F4/5-HDAC1-SUV39H1-DNMT1 complexes, and provided a link between p…

Cancer ResearchTranscription GeneticEstrogen receptorHistone Deacetylase 1HistonesTumor Cells CulturedDNA (Cytosine-5-)-MethyltransferasesReceptorPromoter Regions GeneticE2F4Nuclear ProteinsAcetylationChromatinDNA-Binding ProteinsGene Expression Regulation NeoplasticReceptors Estrogenembryonic structuresDNA methylationFemalepRb2/p130; chromatin-modifying enzymes; estrogen receptor-alpha; breast carcinomabiological phenomena cell phenomena and immunityDNA (Cytosine-5-)-Methyltransferase 1medicine.medical_specialtyanimal structuresmedicine.drug_classMacromolecular SubstancesBreast NeoplasmsE2F4 Transcription FactorBiologyHistone DeacetylasesBreast cancerInternal medicineGeneticsmedicineEstrogen Receptor betaHumansMolecular BiologyEstrogen receptor betaE2F5 Transcription FactorRetinoblastoma-Like Protein p130Estrogen Receptor alphaProteinsMethyltransferasesDNA Methylationmedicine.diseasePhosphoproteinsRepressor Proteinsenzymes and coenzymes (carbohydrates)EndocrinologyEstrogenCancer researchTrans-ActivatorsEstrogen receptor alphaTranscription FactorsOncogene
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Molecular adaptations of the blood–brain barrier promote stress resilience vs. depression

2020

Significance Thirty to fifty percent of depressed individuals are unresponsive to commonly prescribed antidepressant treatments, suggesting that biological mechanisms, such as stress-induced inflammation and blood vessel dysfunction, remain untreated. The blood–brain barrier is the ultimate frontier between the brain and harmful toxins or inflammatory signals circulating in the blood. Depression and vulnerability to chronic social stress are associated with loss of this barrier integrity; however, the mechanisms involved remain poorly understood. Identification of adaptations leading to resilience under stressful conditions could help develop novel treatments. Here we combined behavioral, p…

MaleHistone Deacetylase 1InflammationFOXO1Blood–brain barrierNucleus AccumbensEpigenesis GeneticProinflammatory cytokineMice03 medical and health sciences0302 clinical medicinevascularmedicineAnimalsHumansClaudin-5030304 developmental biologyInflammationSocial stressDepressive Disorder Major0303 health sciencesantidepressantMultidisciplinaryDepressionbusiness.industrySystems BiologyBiological Sciencesmedicine.diseasemood disordersAntidepressive Agents3. Good healthMice Inbred C57BLDisease Models Animalmedicine.anatomical_structureMood disordersBlood-Brain BarrierMajor depressive disorderAntidepressantmedicine.symptombusinessNeuroscienceStress Psychologicalepigenetic030217 neurology & neurosurgerySignal TransductionProceedings of the National Academy of Sciences
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Genetic identification of a network of factors that functionally interact with the nucleosome remodeling ATPase ISWI.

2008

Nucleosome remodeling and covalent modifications of histones play fundamental roles in chromatin structure and function. However, much remains to be learned about how the action of ATP-dependent chromatin remodeling factors and histone-modifying enzymes is coordinated to modulate chromatin organization and transcription. The evolutionarily conserved ATP-dependent chromatin-remodeling factor ISWI plays essential roles in chromosome organization, DNA replication, and transcription regulation. To gain insight into regulation and mechanism of action of ISWI, we conducted an unbiased genetic screen to identify factors with which it interacts in vivo. We found that ISWI interacts with a network o…

MaleProteomicsCancer Researchlcsh:QH426-470Histone Deacetylase 1BiologySettore MED/08 - Anatomia PatologicaChromosomesHistone DeacetylasesChromatin remodelingHistonesHistone H403 medical and health sciences0302 clinical medicineGenetics and Genomics/EpigeneticsGeneticsAnimalsDrosophila ProteinsNucleosomeMolecular BiologyGenetics (clinical)Ecology Evolution Behavior and Systematics030304 developmental biologyAdenosine TriphosphatasesGenetics0303 health sciencesNuclear ProteinsAcetylationChromatin Assembly and DisassemblyChromatinNucleosomesChromatiniswi drosophilaRepressor ProteinsChromatin epigeneticsHDAC Chromatin RemodellingSin3 Histone Deacetylase and Corepressor Complexlcsh:GeneticsDrosophila melanogasterHistoneHistone deacetylase complexbiology.proteinFemaleHistone deacetylaseHistone deacetylase activity030217 neurology & neurosurgeryResearch ArticleTranscription Factors
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Image-Guided Synthesis Reveals Potent Blood-Brain Barrier Permeable Histone Deacetylase Inhibitors

2014

Recent studies have revealed that several histone deacetylase (HDAC) inhibitors, which are used to study/treat brain diseases, show low blood-brain barrier (BBB) penetration. In addition to low HDAC potency and selectivity observed, poor brain penetrance may account for the high doses needed to achieve therapeutic efficacy. Here we report the development and evaluation of highly potent and blood-brain barrier permeable HDAC inhibitors for CNS applications based on an image-guided approach involving the parallel synthesis and radiolabeling of a series of compounds based on the benzamide HDAC inhibitor, MS-275 as a template. BBB penetration was optimized by rapid carbon-11 labeling and PET im…

PhysiologyCognitive NeuroscienceHistone Deacetylase 2Vascular permeabilityHistone Deacetylase 1Blood–brain barrierBiochemistrylaw.inventionCapillary Permeabilitychemistry.chemical_compoundlawmedicineAnimalsHumansCarbon RadioisotopesBenzamideHistone deacetylase 2BrainCell BiologyGeneral MedicinePenetration (firestop)Papio anubisHDAC1Recombinant ProteinsHistone Deacetylase Inhibitorsmedicine.anatomical_structurechemistryBiochemistryBlood-Brain BarrierPositron-Emission TomographyBenzamidesRecombinant DNABiophysicsDrug EvaluationFemaleHistone deacetylaseRadiopharmaceuticals
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The histone deacetylase Rpd3 regulates the heterochromatin structure of Drosophila telomeres

2011

Telomeres are specialized structures at the end of eukaryotic chromosomes that are required to preserve genome integrity, chromosome stability and nuclear architecture. Telomere maintenance and function are established epigenetically in several eukaryotes. However, the exact chromatin enzymatic modifications regulating telomere homeostasis are poorly understood. In Drosophila melanogaster, telomere length and stability are maintained through the retrotransposition of specialized telomeric sequences and by the specific loading of protecting capping proteins, respectively. Here, we show that the loss of the essential and evolutionarily conserved histone deacetylase Rpd3, the homolog of mammal…

Telomere-binding proteinGeneticsEpigenomicsMaleHistone deacetylase 5Histone deacetylase 2HDAC11Histone Deacetylase 1Cell BiologyBiologyTelomereHistone H4Telomere HomeostasisDrosophila melanogasterHeterochromatinHistone H2Ahistone deacetylaseHistone codeAnimalsDrosophila Proteinsanimals; article; chromosome aberration; chromosome structure; drosophila; drosophila melanogaster; drosophila proteins; enzyme activity; epigenetics; epigenomics; eukaryota; heterochromatin; histone acetylation; histone deacetylase 1; histone deacetylase rpd 3; histone methylation; male; mammalia; nonhuman; polytene chromosome; priority journal; regulatory mechanism; telomere; unclassified drugPolytene Chromosomes
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