Search results for "Deacetylase inhibitor."

showing 10 items of 73 documents

Inhibition of class I histone deacetylase with an apicidin derivative prevents cardiac hypertrophy and failure

2008

AIMS: Recent studies have demonstrated the importance of chromatin remodelling via histone acetylation/deacetylation for the control of cardiac gene expression. Specific histone deacetylases (HDACs) can, in fact, play a positive or negative role in determining cardiac myocyte (CM) size. Here, we report on the effect on hypertrophy development of three inhibitors (HDACi) of class I HDACs. METHODS AND RESULTS: The compounds were first analysed in vitro by scoring hypertrophy, expression of foetal genes, and apoptosis of neonatal rat CMs stimulated with phenylephrine, an alpha1-adrenergic agonist. This initial screening indicated that a truncated derivative of apicidin with class I HDAC specif…

Cardiac function curvemedicine.medical_specialtyHypertrophy Heart failurePhysiologymedicine.drug_classBiologyPeptides CyclicHistone DeacetylasesCell LineMuscle hypertrophychemistry.chemical_compoundPhysiology (medical)Internal medicinemedicineAnimalsHumansMyocytes CardiacEnzyme InhibitorsRats WistarCells CulturedHeart FailurePressure overloadHistone deacetylase inhibitorHypertrophic cardiomyopathyHypertrophymedicine.diseaseRatsHistone Deacetylase InhibitorsDisease Models AnimalEndocrinologychemistryEchocardiographyHeart failureHypertrophy Left VentricularHistone deacetylaseCardiology and Cardiovascular MedicineApicidinCardiovascular Research
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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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Transcription of genes in the biosynthetic pathway for fumonisin mycotoxins is epigenetically and differentially regulated in the fungal maize pathog…

2012

ABSTRACT When the fungal pathogen Gibberella moniliformis (anamorph, Fusarium verticillioides ) colonizes maize and maize-based products, it produces class B fumonisin (FB) mycotoxins, which are a significant threat to human and animal health. FB biosynthetic enzymes and accessory proteins are encoded by a set of clustered and cotranscribed genes collectively named FUM, whose molecular regulation is beginning to be unraveled by researchers. FB accumulation correlates with the amount of transcripts from the key FUM genes, FUM1 , FUM21 , and FUM8 . In fungi in general, gene expression is often partially controlled at the chromatin level in secondary metabolism; when this is the case, the deac…

DISRUPTIONTranscription GeneticFUM21[SDV]Life Sciences [q-bio]DIVERSITYPROTEINFusarium verticillioidesmaizeSECONDARY METABOLISMgene clusterEpigenesis GeneticHistonesFUM8FusariumGene Expression Regulation FungalASPERGILLUSPromoter Regions Genetic2. Zero hungerGenetics0303 health sciencesHistone deacetylase inhibitorhistone acetylationAcetylationArticlesGeneral MedicineChromatinChromatinGENOMEHistoneMultigene Family[SDE]Environmental SciencesTrichostatin AEpigenetics; Fusarium verticillioides; fmonisin synthesismedicine.drugCONIDIATIONChromatin Immunoprecipitationmedicine.drug_classGenes FungalChIPBiologyGFPZea maysMicrobiologyFumonisinsChromatin remodeling03 medical and health sciencesmedicineEpigeneticsMolecular Biology030304 developmental biologyepigenetics030306 microbiologyCLUSTERFumonisins; epigenetics; Fusarium verticillioides; maize; histone acetylation; histone deacetylases; ChIP; Trichostatin A; FUM1; FUM21; FUM8; GFP; gene clusterMycotoxinsChromatin Assembly and DisassemblyFUM1Histone Deacetylase InhibitorsTrichostatin AAcetylationbiology.proteinChromatin immunoprecipitationhistone deacetylases
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Antitumor Effects of a Combined 5-Aza-2′Deoxycytidine and Valproic Acid Treatment on Rhabdomyosarcoma and Medulloblastoma in Ptch Mutant Mice

2009

Abstract Patched (Ptch) heterozygous mice develop medulloblastoma (MB) and rhabdomyosarcoma (RMS) resembling the corresponding human tumors. We have previously shown that epigenetic silencing of the intact Ptch allele contributes to tumor formation in this model. Here, we investigated whether targeting of epigenetic silencing mechanisms could be useful in the treatment of Ptch-associated cancers. A reduction of endogenous DNA methyltransferase1 (Dnmt1) activity significantly reduced tumor incidence in heterozygous Ptch knockout mice. A combined treatment with the Dnmt inhibitor 5-aza-2′deoxycytidine (5-aza-dC) and the histone deacetlyase (HDAC) inhibitor valproic acid (VPA) efficiently prev…

DNA (Cytosine-5-)-Methyltransferase 1Patched ReceptorsPatchedCancer Researchmedicine.drug_classGene ExpressionDecitabineReceptors Cell SurfaceBiologyDecitabineHistone DeacetylasesHistonesMice03 medical and health sciences0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsRhabdomyosarcomamedicineAnimalsDNA (Cytosine-5-)-MethyltransferasesGene SilencingMuscle SkeletalRhabdomyosarcoma030304 developmental biologyMedulloblastomaMice Inbred BALB C0303 health sciencesValproic AcidHistone deacetylase inhibitorCancerAcetylationDNA Methylationmedicine.disease3. Good healthHistone Deacetylase InhibitorsMice Inbred C57BLPatched-1 Receptorstomatognathic diseasesOncology030220 oncology & carcinogenesisAzacitidineCancer researchDNMT1Epigenetic therapyMedulloblastomamedicine.drugCancer Research
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Influences of histone deacetylase inhibitors and resveratrol on DNA repair and chromatin compaction

2013

Accessibility of DNA is a prerequisite for both DNA damage and repair. Therefore, the chromatin structure is expected to have major impact on both processes, with opposite consequences for the stability of the genome. To analyse the influence of chromatin compaction on the generation and repair of various types of DNA modifications, we modulated the global chromatin structure of AS52 Chinese hamster ovary cells and HeLa cells by treatment with either histone deacetylase inhibitors or resveratrol and measured the repair kinetics of (i) pyrimidine dimers induced by ultraviolet B, (ii) oxidised purines generated by photosensitisation and (iii) single-strand breaks induced by H2O2, using an alk…

DNA RepairUltraviolet RaysDNA damageDNA repairHealth Toxicology and MutagenesisCarbazolesCHO CellsHydroxamic AcidsToxicologyChromatin remodelingCricetulusStilbenesHistone H2AGeneticsmedicineAnimalsDeoxyribonuclease IHumansDNA Breaks Single-StrandedGenetics (clinical)EpigenomicsbiologyChemistryMolecular biologyChromatinCell biologyProliferating cell nuclear antigenChromatinHistone Deacetylase InhibitorsButyratesTrichostatin APyrimidine DimersResveratrolbiology.proteinHeLa Cellsmedicine.drugMutagenesis
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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 JAHA Down-Regulates pERK and Global DNA Methylation in MDA-MB231 Breast Cancer Cells

2015

The histone deacetylase inhibitor N-1-(ferrocenyl)-N-8-hydroxyoctanediamide (JAHA) down-regulates extracellular-signal-regulated kinase (ERK) and its activated form in triple-negative MDA-MB231 breast cancer cells after 18 h and up to 30 h of treatment, and to a lesser extent AKT and phospho-AKT after 30 h and up to 48 h of treatment. Also, DNA methyltransferase 1 (DNMT1), 3b and, to a lesser extent, 3a, downstream ERK targets, were down-regulated already at 18 h with an increase up to 48 h of exposure. Methylation-sensitive restriction arbitrarily-primed (MeSAP) polymerase chain reaction (PCR) analysis confirmed the ability of JAHA to induce genome-wide DNA hypomethylation at 48 h of expos…

DNA methyltransferase (DNMT)medicine.drug_classDNA methyltransferaselcsh:TechnologymedicineGeneral Materials ScienceCancer epigeneticsSettore BIO/06 - Anatomia Comparata E Citologialcsh:Microscopyhistone deacetylase inhibitorlcsh:QC120-168.85QD0415Histone deacetylase 5lcsh:QH201-278.5extracellular-signal-regulated kinase (ERK)ChemistryHistone deacetylase 2lcsh:TCommunicationAKTHistone deacetylase inhibitorMolecular biologySettore BIO/18 - Geneticalcsh:TA1-2040DNA methylationDNMT1lcsh:Descriptive and experimental mechanicslcsh:Electrical engineering. Electronics. Nuclear engineeringlcsh:Engineering (General). Civil engineering (General)lcsh:TK1-9971DNA hypomethylationQD0241
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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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