Search results for "HDAC"

showing 10 items of 72 documents

Properties of the yeast nuclear histone deacetylase.

1994

A nuclear histone deacetylase from yeast was partially purified and some of its characteristics were studied. Histone deacetylase activity was stimulated in vitro by high-mobility-group nonhistone chromatin proteins 1 and 2 and ubiquitin and inhibited by spermine and spermidine, whereas n-butyrate had no significant inhibitory effect. Like the mammalian enzyme, partially purified histone deacetylase from yeast was strongly inhibited by trichostatin A. However, in crude extract preparations the yeast enzyme was not inhibited and treatment with trichostatin in vivo did not show any effect, either on the histone acetylation level or on cell viability. At low ionic strength, the enzyme can be i…

Cell NucleusHistone deacetylase 5HDAC11ChemistryHistone deacetylase 2HDAC10Cell BiologySaccharomyces cerevisiaeHydroxamic AcidsBiochemistryHistone DeacetylasesSubstrate SpecificityHistone Deacetylase InhibitorsMolecular WeightTrichostatin ABiochemistrymedicineChromatography GelHistone deacetylase activityHistone deacetylaseMolecular Biologymedicine.drugDeacetylase activityResearch ArticleThe Biochemical journal
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A novel moniliformin derivative as pan-inhibitor of histone deacetylases triggering apoptosis of leukemia cells

2021

New and potent agents that evade multidrug resistance (MDR) and inhibit epigenetic modifications are of great interest in cancer drug development. Here, we describe that a moniliformin derivative (IUPAC name: 3-(naphthalen-2-ylsulfanyl)-4-{[(2Z)-1,3,3-trimethyl-2,3-dihydro-1H-indol-2-ylidene]methyl}cyclobut-3-ene-1,2-dione; code: MCC1381) bypasses P-gp-mediated MDR. Using transcriptomics, we identified a large number of genes significantly regulated in response to MCC1381, which affected the cell cycle and disturbed cellular death and survival. The potential targets of MCC1381 might be histone deacetylases (HDACs) as predicted by SwissTargetPrediction. In silico studies confirmed that MCC13…

Cell SurvivalApoptosisBiochemistryHistone DeacetylasesProtein Structure SecondaryAnimalsHumansEpigeneticsZebrafishP-glycoproteinPharmacologyLeukemiaDose-Response Relationship DrugbiologyChemistryMycotoxinsCell cycleHDAC6HCT116 CellsXenograft Model Antitumor AssaysProtein Structure TertiaryCell biologyHistone Deacetylase InhibitorsMolecular Docking SimulationHEK293 CellsHistoneAcetylationApoptosisCancer cellbiology.proteinCyclobutanesBiochemical Pharmacology
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Class 1 Histone Deacetylases and Ataxia-Telangiectasia Mutated Kinase Control the Survival of Murine Pancreatic Cancer Cells upon dNTP Depletion

2021

Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive disease with a dismal prognosis. Here, we show how an inhibition of de novo dNTP synthesis by the ribonucleotide reductase (RNR) inhibitor hydroxyurea and an inhibition of epigenetic modifiers of the histone deacetylase (HDAC) family affect short-term cultured primary murine PDAC cells. We used clinically relevant doses of hydroxyurea and the class 1 HDAC inhibitor entinostat. We analyzed the cells by flow cytometry and immunoblot. Regarding the induction of apoptosis and DNA replication stress, hydroxyurea and the novel RNR inhibitor COH29 are superior to the topoisomerase-1 inhibitor irinotecan which is used to treat PDAC. Ent…

DNA Replicationendocrine system diseasesDNA damagereplication stressQH301-705.5RNR Inhibitor COH29Antineoplastic AgentsCell Cycle ProteinsRNRAtaxia Telangiectasia Mutated ProteinsArticle03 medical and health scienceschemistry.chemical_compoundAtaxia TelangiectasiaMice0302 clinical medicineHDACAnimalscancerPDAC cellsRibonucleotide Reductase SubunitEnzyme InhibitorsBiology (General)030304 developmental biology0303 health sciencesbiologyChemistryEntinostatDNA replicationapoptosisGeneral Medicine3. Good healthPancreatic NeoplasmsHistoneRibonucleotide reductase030220 oncology & carcinogenesisATMbiology.proteinCancer researchDNA damageHistone deacetylaseCells
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In Vitro Assessment of the Genotoxic Hazard of Novel Hydroxamic Acid- and Benzamide-Type Histone Deacetylase Inhibitors (HDACi)

2020

Histone deacetylase inhibitors (HDACi) are already approved for the therapy of leukemias. Since they are also emerging candidate compounds for the treatment of non-malignant diseases, HDACi with a wide therapeutic window and low hazard potential are desirable. Here, we investigated a panel of 12 novel hydroxamic acid- and benzamide-type HDACi employing non-malignant V79 hamster cells as toxicology guideline-conform in vitro model. HDACi causing a &ge

DNA damageApoptosisHydroxamic AcidsDNA damage responseArticleCatalysisCell LineHistonesInorganic Chemistrylcsh:Chemistrychemistry.chemical_compoundHDAC inhibitorsCricetinaeDNA strand breaksmedicineAnimalsHumansDNA Breaks Double-StrandedDNA Breaks Single-StrandedPhosphorylationPhysical and Theoretical Chemistrynormal tissue toxicityMolecular BiologyVorinostatlcsh:QH301-705.5SpectroscopyVorinostatMicronucleus TestsHydroxamic acidMutagenicity TestsEntinostatOrganic ChemistryHistone H2AXgenetic instabilityGeneral MedicineComputer Science ApplicationsHistone Deacetylase Inhibitorschemistrylcsh:Biology (General)lcsh:QD1-999BenzamidesCancer researchComet AssayHistone deacetylasegenotoxic hazardDNAMutagensNucleotide excision repairmedicine.drugInternational Journal of Molecular Sciences
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The histone deacetylase inhibitor suberoylanilide hydroxamic acid sensitizes human hepatocellular carcinoma cells to TRAIL-induced apoptosis by TRAIL…

2009

Abstract This paper shows that the histone deacetylase inhibitor SAHA sensitised at sub-toxic doses human hepatocellular carcinoma cells (HepG2, Hep3B and SK-Hep1) to TRAIL-induced apoptosis, while it was ineffective in primary human hepatocytes (PHHs). In particular in HCC cells SAHA increased the expression of death receptor 5 (DR5) and caused a decrement of c-Flip. These two modifications provoked in the presence of TRAIL the rapid production of TRAIL-DISC and the activation of caspase-8. Consequently SAHA/TRAIL combination induced many apoptotic events, such as a cleavage of Bid into tBid, dissipation of mitochondrial membrane potential, activation of caspase-3 with the consequent cleav…

Death Domain Receptor Signaling Adaptor ProteinsCancer Researchmedicine.medical_specialtyProgrammed cell deathCarcinoma Hepatocellularmedicine.drug_classmedicine.medical_treatmentBlotting WesternCASP8 and FADD-Like Apoptosis Regulating ProteinDown-RegulationAntineoplastic AgentsApoptosisBiologyHydroxamic AcidsHDACI TRAIL apoptosisInternal medicineSettore BIO/10 - BiochimicamedicineHumansProtein kinase BVorinostatLiver NeoplasmsHistone deacetylase inhibitorNF-kappa Bmedicine.diseaseReceptors TNF-Related Apoptosis-Inducing LigandCytokineEndocrinologyOncologyDrug Resistance NeoplasmApoptosisHepatocellular carcinomaCancer researchTumor necrosis factor alphaSignal transductionProto-Oncogene Proteins c-akt
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From the covalent linkage of drugs to novel inhibitors of ribonucleotide reductase: synthesis and biological evaluation of valproic esters of 3'-C-me…

2014

We synthesized a series of serum-stable covalently linked drugs derived from 3'-C-methyladenosine (3'-Me-Ado) and valproic acid (VPA), which are ribonucleotide reductase (RR) and histone deacetylase (HDAC) inhibitors, respectively. While the combination of free VPA and 3'-Me-Ado resulted in a clear synergistic apoptotic effect, the conjugates had lost their HDAC inhibitory effect as well as the corresponding apoptotic activity. Two of the analogs, 2',5'-bis-O-valproyl-3'-C-methyladenosine (A160) and 5'-O-valproyl-3'-C-methyladenosine (A167), showed promising cytotoxic activities against human hematological and solid cancer cell lines. A167 was less potent than A160 but had interesting featu…

Deoxyribonucleoside triphosphateAdenosineCell SurvivalClinical BiochemistryAllosteric regulationPharmaceutical ScienceAntineoplastic AgentsPharmacologyBiochemistryHistone deacetylase (HDAC) inhibitorHistone DeacetylasesAdenosine TriphosphateAllosteric RegulationCell Line TumorDrug DiscoveryRibonucleotide ReductasesmedicineValproic acidHumansRibonucleotide reductase (RR) inhibitorEnzyme InhibitorsMolecular Biology3′-C-methyladenosineNucleoside analogueKinaseChemistryOrganic ChemistryApoptosiEstersSettore CHIM/08 - Chimica FarmaceuticaHematological and solid tumorHistone Deacetylase InhibitorsKineticsRibonucleotide reductaseBiochemistrySettore BIO/14 - FarmacologiaMolecular MedicineHistone deacetylaseNucleosideIntracellularmedicine.drug
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Characterization of the NAD-Dependent Human Histone Deacetylases Gene Sirtuin 1 and Its Implications on Aging and the Development of Malignant Diseas…

2006

Abstract A dysregulation of the tightly controlled equilibrium of acetylation and deacetylation plays a causative role in the generation as well as in the suppression of cancer. Histone acetylation modifiers are therefore gaining increasing attention as potential targets in the treatment of cancer. Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, which belongs to the silent information regulator 2 (Sir2) family of sirtuin histone deacetylases (HDACs). The yeast Sir2 protein and its mammalian derivatives play a central role in epigenetic gene silencing, DNA repair and recombination, cell-cycle, microtubule organization, and in the regulation of aging. We…

GeneticsHistone deacetylase 5biologyHDAC11Sirtuin 1Histone deacetylase 2ImmunologyCell BiologyHematologySAP30BiochemistryHDAC4biology.proteinHistone codeHistone deacetylaseBlood
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Redox regulation of genome stability by effects on gene expression, epigenetic pathways and DNA damage/repair

2015

Reactive oxygen and nitrogen species (e.g. H2O2, nitric oxide) confer redox regulation of essential cellular signaling pathways such as cell differentiation, proliferation, migration and apoptosis. In addition, classical regulation of gene expression or activity, including gene transcription to RNA followed by translation to the protein level, by transcription factors (e.g. NF-κB, HIF-1α) and mRNA binding proteins (e.g. GAPDH, HuR) is subject to redox regulation. This review will give an update of recent discoveries in this field, and specifically highlight the impact of reactive oxygen and nitrogen species on DNA repair systems that contribute to genomic stability. Emphasis will be placed …

Genome instabilityRedox signalingRNA UntranslatedEpigenetic regulation of neurogenesisDNA RepairHuR mRNA-binding protein in the 3′-untranslated regionClinical BiochemistryHDAC histone deacetylaseReview ArticleAP-1 activator protein 1BiochemistryApe-1 apurinic/apyrimidinic endonuclease 1GPx-1 glutathione peroxidase-1Epigenesis GeneticHistonesTrx thioredoxinPHD prolylhydroxylaseBER base excision repairlcsh:QH301-705.5HO-1 heme oxygenase-1EpigenomicsGeneticsRegulation of gene expressionNox member of the NADPH oxidase familylcsh:R5-920JmjC Jumonji C domain-containing histone demethylasesHIF-1α hypoxia inducible factor-1α5-hmC 5-hydroxymethylcytosineddc:Cell biologyMMP matrix metalloproteinaseGrx glutaredoxinGAPDH glyceraldehyde-3-phosphate dehydrogenaseNrf2 nuclear factor erythroid related factor 2DNA methylationEpigeneticslcsh:Medicine (General)Oxidation-ReductionSignal Transduction5-mC 5-methylcytosineDNA repairDNA damageNF-κB nuclear factor-κBBiologyGenomic InstabilityRNS reactive nitrogen speciesROS reactive oxygen speciesNER nucleotide excision repairSOD superoxide dismutaseOxyR transcription factor (hydrogen peroxide-inducible genes activator)HumansEpigeneticsOrganic ChemistryPETN pentaerithrityl tetranitrateGene regulationOxidative StressDNMT DNA methyltransferaseGene Expression Regulationlcsh:Biology (General)AREs AU-rich elementsHAT histone acetyltransferaseKeap1 kelch-like ECH-associated protein 1BiomarkersCOPD chronic obstructive pulmonary disorderDNA DamageRedox Biology
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IκB kinase-driven nuclear factor-κB activation in patients with asthma and chronic obstructive pulmonary disease.

2011

Background Nuclear factor-κB (NF-κB) is a transcriptional factor of different inflammatory patterns involved in asthma and chronic obstructive pulmonary disease (COPD) that is tightly controlled by IκB kinase (IKK) complex. Objective We investigated the dysregulation of IKK-driven NF-κB activation in patients with asthma and COPD. Methods We assessed IKKα and IKKβ expression and activation, their regulation by glucocorticosteroids, and their involvement in IL-8 synthesis in PBMCs isolated from asthmatic patients, healthy smokers (HSs), patients with COPD, and control subjects. PBMCs from control subjects were stimulated with TNF-α and cigarette smoke extract in the presence or absence of fl…

Glutathione-S-transferaseAdultMaleImmunologyInflammationIκB kinaseFluticasone propionateFEV1/FVC ratioPulmonary Disease Chronic ObstructiveImmunopathologymedicineImmunology and AllergyHumansInterleukin 8COPD CSE Fluticasone propionateIKK IκB kinaseGlucocorticoidsAsthmaHDACCOPDbusiness.industryInterleukin-8SmokingNF-kappa BMiddle Agedmedicine.diseaseAsthmaBronchodilator AgentsI-kappa B KinaseEnzyme ActivationGene Expression RegulationNF-κBImmunologyLeukocytes MononuclearFemalemedicine.symptombusinessmedicine.drugThe Journal of allergy and clinical immunology
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La Perdita di Funzione del Complesso di Deacetilazione Istonica Sin3A/Rpd3 Causa Fusioni Telomeriche

2008

HDAC Sin3A Rpd3 chromatin
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