Search results for "DNA Modification"

showing 10 items of 31 documents

Synthesis and in Vitro Evaluation of Biotinylated RG108:  A High Affinity Compound for Studying Binding Interactions with Human DNA Methyltransferases

2006

Small-molecule inhibitors of DNA methyltransferases such as RG108 represent promising candidates for cancer drug development. We report the synthesis and in vitro analysis of a biotinylated RG108 conjugate, 2-(1,3-dioxo-1,3-dihydro-isoindol-2-yl)-3-(5-[3-[5-(2-oxo-hexahydro-thieno[3,4-d]imidazol-4-yl)pentanoylamino]propoxy]-1H-indol-3-yl)propionic acid (bio-RG108), for the evaluation of interactions with DNA methyltransferase enzymes. The structural design of the chemically modified inhibitor was aided by molecular modeling, which suggested the possibility for extensive chemical modifications at the 5-position of the tryptophan moiety in RG108. The inhibitory activity of the corresponding d…

IndolesMethyltransferaseMolecular modelStereochemistryBiomedical EngineeringBiotinPharmaceutical SciencePhthalimidesBioengineeringDNA methyltransferaseCell-free systemchemistry.chemical_compoundAffinity chromatographyHumansDNA Modification MethylasesNuclear Magnetic Resonance BiomolecularPharmacologychemistry.chemical_classificationCell-Free SystemMolecular StructureChemistryOrganic ChemistryTryptophanEnzymeBiochemistryBiotinylationPropionatesDNAProtein BindingBiotechnologyBioconjugate Chemistry
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Early impairment of epigenetic pattern in neurodegeneration: Additional mechanisms behind pyrethroid toxicity

2019

Abstract Permethrin is a synthetic pyrethroid extensively used as anti-woodworm agent and for indoor and outdoor pest control. The main route of human exposure is through fruit, vegetable and milk intake. Low dosage exposure to permethrin during neonatal brain development (from postnatal day 6 to postnatal day 21) leads to dopamine decrease in rat striatum nucleus, oxidative stress and behavioural changes linked to the development of Parkinson's like neurodegeneration later in life. The aim of this study was to evaluate the expression of genes involved in the dopaminergic pathway and epigenetic regulatory mechanisms in adolescent rats treated with permethrin during neonatal brain developmen…

Male0301 basic medicineAgingDopamineStriatumPharmacologyBiologyBiochemistryEpigenesis GeneticMECP203 medical and health sciences0302 clinical medicineEndocrinologyDopamineNuclear Receptor Subfamily 4 Group A Member 2parasitic diseasesGeneticsmedicineAnimalsEpigeneticsRats WistarPromoter Regions GeneticDNA Modification MethylasesMolecular BiologyPermethrinOrphan receptorDopaminergicNeurodegenerationNeurodegenerative DiseasesCell BiologyDNA Methylationmedicine.diseaseCorpus StriatumRatsMolecular Docking Simulation030104 developmental biologyAnimals Newbornalpha-SynucleinProtein Multimerization030217 neurology & neurosurgeryPermethrinmedicine.drugExperimental Gerontology
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Abnormal Hypermethylation at Imprinting Control Regions in Patients with S-Adenosylhomocysteine Hydrolase (AHCY) Deficiency

2016

S-adenosylhomocysteine hydrolase (AHCY) deficiency is a rare autosomal recessive disorder in methionine metabolism caused by mutations in the AHCY gene. Main characteristics are psychomotor delay including delayed myelination and myopathy (hypotonia, absent tendon reflexes etc.) from birth, mostly associated with hypermethioninaemia, elevated serum creatine kinase levels and increased genome wide DNA methylation. The prime function of AHCY is to hydrolyse and efficiently remove S-adenosylhomocysteine, the by-product of transmethylation reactions and one of the most potent methyltransferase inhibitors. In this study, we set out to more specifically characterize DNA methylation changes in blo…

Male0301 basic medicineMethyltransferaselcsh:MedicineArtificial Gene Amplification and ExtensionGlycine N-MethyltransferaseBiochemistryPolymerase Chain Reactionlaw.inventionMethionine0302 clinical medicinelawAmino Acidslcsh:SciencePolymerase chain reactionGeneticsDNA methylationMammalian GenomicsMultidisciplinaryOrganic CompoundsGenomicsMethylationChromatinEnzymes3. Good healthNucleic acidsChemistryPhysical SciencesDNA methylationEpigeneticsFemaleDNA modificationChromatin modificationResearch ArticleChromosome biologyCell biologyAlu elementBiologyResearch and Analysis MethodsGenomic Imprinting03 medical and health sciencesAlu ElementsGeneticsSulfur Containing Amino AcidsHumansRepeated SequencesMolecular Biology TechniquesMolecular BiologyAmino Acid Metabolism Inborn ErrorsGeneBiology and life sciencesOrganic Chemistrylcsh:RChemical CompoundsInfant NewbornProteinsInfantDNAMethyltransferasesCreatineMolecular biologyLong Interspersed Nucleotide Elements030104 developmental biologyDifferentially methylated regionsAnimal GenomicsEnzymologyAHCY ; Hypermethylationlcsh:QGene expressionGenomic imprinting030217 neurology & neurosurgeryDevelopmental BiologyPLOS ONE
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Epigenetic outlier profiles in depression: A genome-wide DNA methylation analysis of monozygotic twins

2018

Recent discoveries highlight the importance of stochastic epigenetic changes, as indexed by epigenetic outlier DNA methylation signatures, as a valuable tool to understand aberrant cell function and subsequent human pathology. There is evidence of such changes in different complex disorders as diverse as cancer, obesity and, to a lesser extent, depression. The current study was aimed at identifying outlying DNA methylation signatures of depressive psychopathology. Here, genome-wide DNA methylation levels were measured (by means of Illumina Infinium HumanMethylation450 Beadchip) in peripheral blood of thirty-four monozygotic twins informative for depressive psychopathology (lifetime DSM-IV d…

Male0301 basic medicineTwinslcsh:MedicineBiochemistryGenomeEpigenesis GeneticDatabase and Informatics MethodsMedicine and Health SciencesDepressió psíquicalcsh:ScienceEpigenesisGeneticsDNA methylationMultidisciplinaryDepressionGenomicsMethylationMiddle AgedChromatinNucleic acidsMental depressionCpG sitePhysical SciencesDNA methylationBessonsEpigeneticsFemalegenoma humàDNA modificationChromatin modificationResearch ArticleChromosome biologyStatistical DistributionsAdultCell biologyHealth InformaticsGenomicsBiologyResearch and Analysis MethodsPolymorphism Single Nucleotidemalalties mentalsYoung Adult03 medical and health sciencesMental Health and PsychiatryGeneticsHumansEpigeneticsGeneTreatment GuidelinesHealth Care PolicyBiology and life sciencesMood Disorderslcsh:RDNATwins MonozygoticEpigenèticaProbability TheoryExpressió gènicaHealth Care030104 developmental biologylcsh:QCpG IslandsGene expressionMathematicsDevelopmental Biology
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Inhibition of DNA methylation sensitizes glioblastoma for tumor necrosis factor-related apoptosis-inducing ligand-mediated destruction.

2005

AbstractLife expectancy of patients affected by glioblastoma multiforme is extremely low. The therapeutic use of tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) has been proposed to treat this disease based on its ability to kill glioma cell lines in vitro and in vivo. Here, we show that, differently from glioma cell lines, glioblastoma multiforme tumors were resistant to TRAIL stimulation because they expressed low levels of caspase-8 and high levels of the death receptor inhibitor PED/PEA-15. Inhibition of methyltransferases by decitabine resulted in considerable up-regulation of TRAIL receptor-1 and caspase-8, down-regulation of PED/PEA-15, inhibition of cell growth, and …

MaleCancer ResearchMethyltransferaseNudeDrug ResistanceApoptosisReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandCASPASE-8 EXPRESSIONMiceNude mouseSIGNALING COMPLEXReceptorsAntineoplastic Combined Chemotherapy ProtocolsTumor Cells CulturedDNA Modification MethylasesIN-VIVOHeterologousCaspase 8CulturedMembrane GlycoproteinsbiologyIntracellular Signaling Peptides and ProteinsMiddle AgedTumor CellsGene Expression Regulation NeoplasticMALIGNANT GLIOMA-CELLSOncologyCaspasesDNA methylationAzacitidineTumor necrosis factor alphaFemalemedicine.drugSignal TransductionAdultBRAIN-TUMORSTransplantation HeterologousCHEMOTHERAPEUTIC-AGENTSDecitabineMice NudeDecitabineDRUG-INDUCED APOPTOSISDEATH RECEPTOR5-AZA-2'-DEOXYCYTIDINEIn vivoSettore MED/04 - PATOLOGIA GENERALEmedicineAnimalsHumansneoplasmsAgedTransplantationNeoplasticCell growthTumor Necrosis Factor-alphaHistocompatibility Antigens Class IDNA Methylationbiology.organism_classificationPhosphoproteinsReceptors TNF-Related Apoptosis-Inducing LigandGene Expression RegulationApoptosisDrug Resistance NeoplasmImmunologyCancer researchNeoplasmAdult; Aged; Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Apoptosis Regulatory Proteins; Azacitidine; Caspase 8; Caspases; DNA Modification Methylases; Drug Resistance Neoplasm; Female; Glioblastoma; Histocompatibility Antigens Class I; Humans; Intracellular Signaling Peptides and Proteins; Male; Membrane Glycoproteins; Mice; Mice Nude; Middle Aged; Phosphoproteins; Receptors TNF-Related Apoptosis-Inducing Ligand; Receptors Tumor Necrosis Factor; Signal Transduction; TNF-Related Apoptosis-Inducing Ligand; Transplantation Heterologous; Tumor Cells Cultured; Tumor Necrosis Factor-alpha; DNA Methylation; Gene Expression Regulation Neoplastic; Cancer Research; OncologyTumor Necrosis FactorTRAIL-INDUCED APOPTOSISApoptosis Regulatory ProteinsGlioblastomaCancer research
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Promoter methylation of MGMT, MLH1 and RASSF1A tumor suppressor genes in head and neck squamous cell carcinoma: Pharmacological genome demethylation …

2012

Promoter hypermethylation of tumor suppressor genes (TSGs) is a common feature of primary cancer cells. However, to date the somatic epigenetic events that occur in head and neck squamous cell carcinoma (HNSCC) tumorigenesis have not been well-defined. In the present study, we analyzed the promoter methylation status of the genes mutL homolog 1 (MLH1), Ras-association domain family member 1 (RASSF1A) and O-6-methylguanine-DNA methyltransferase (MGMT) in 23 HNSCC samples, three control tissues and one HNSCC cell line (UM-SCC 33) using methylation-specific PCR (MSP). The expression of the three proteins was quantified by semi-quantitative immunohistochemical analysis. The cell line was treate…

MaleCancer Researchmedicine.disease_causePolymerase Chain Reactionchemistry.chemical_compoundRas association domain family member 1Genes Tumor Suppressortumor suppressor geneEnzyme InhibitorsPromoter Regions GeneticDNA Modification MethylasesAged 80 and overNuclear ProteinsArticlesGeneral MedicineMethylationMiddle AgedImmunohistochemistryPrimary tumorOncologyDealkylationHead and Neck NeoplasmsDNA methylationAzacitidineCarcinoma Squamous CellFemaleMutL Protein Homolog 1Molecular Sequence DataDown-RegulationBiologyhead and neck squamous cell carcinomamutL homolog 15-azacytidineCell Line TumormedicineHumansEpigeneticsneoplasmsO-6-methylguanine-DNA methyltransferaseAdaptor Proteins Signal TransducingAgedCell ProliferationBase SequenceDose-Response Relationship DrugTumor Suppressor ProteinsSequence Analysis DNADNA Methylationmedicine.diseaseHead and neck squamous-cell carcinomaMolecular biologyDemethylating agentSquamous carcinomastomatognathic diseasesDNA Repair EnzymeschemistryCase-Control StudiesCpG IslandsCarcinogenesisOncology Reports
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Immunoprofiles and DNA methylation of inflammatory marker genes in ulcerative colitis-associated colorectal tumorigenesis

2021

Immunological and epigenetic changes are interconnected and contribute to tumorigenesis. We determined the immunoprofiles and promoter methylation of inflammation-related genes for colitis-associated colorectal carcinomas (CA-CRC). The results were compared with Lynch syndrome (LS)-associated colorectal tumors, which are characterized by an active immune environment through inherited mismatch repair defects. CA-CRCs (n = 31) were immunohistochemically evaluated for immune cell scores (ICSs) and PDCD1 and CD274 expression. Seven inflammation-associated genes (CD274, NTSR1, PPARG, PTGS2, PYCARD, SOCS1, and SOCS2), the repair gene MGMT, and eight standard marker genes for the CpG Island Methyl…

MaleCarcinogenesismedicine.disease_causeBiochemistry0302 clinical medicineIntestinal MucosaDNA Modification Methylases0303 health sciencesMUCOSADNA methylationtulehdusinflammation-associated genesPYCARDMethylationMiddle AgedLynch syndromeQR1-502EPIGENETICS3. Good healthDNA-metylaatioGene Expression Regulation NeoplasticPhenotypecolon cancerepigenetiikka030220 oncology & carcinogenesisimmuunivasteDNA methylationFemaleColorectal NeoplasmsCANCERSINSTABILITYsuolistosyövätBiology3121 Internal medicineMicrobiologyArticle03 medical and health sciencesmedicineHumansEpigeneticsLynchin oireyhtymäMolecular Biologyneoplasms030304 developmental biologypaksusuolisyöpäulcerative colitisInflammationCpG Island Methylator PhenotypeTumor Suppressor Proteinshaavainen koliittimedicine.disease3126 Surgery anesthesiology intensive care radiologydigestive system diseasesDNA Repair EnzymesLynch syndrome3121 General medicine internal medicine and other clinical medicineMutationimmune cell scoreCancer research1182 Biochemistry cell and molecular biologyColitis UlcerativeCpG IslandsField cancerizationCarcinogenesisBiomarkers
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Coffee and its chemopreventive components Kahweol and Cafestol increase the activity of O6-methylguanine-DNA methyltransferase in rat liver—compariso…

2003

Abstract A lower rate of colon cancer was observed in consumers of coffee with a high content of the diterpenes Kahweol and Cafestol (K/C). In animal models, K/C have been found to protect against the mutagenic/carcinogenic effects of compounds such as 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), aflatoxin B1, and 7,12-dimethylbenz[a]anthracene. Thus far, such chemoprotection by K/C has been attributed to modifications of xenobiotic metabolism, e.g. enhanced detoxification by UDP-glucuronosyltransferase (UDPGT) and/or glutathione transferase (GST). In the present study, we investigated the potential of several coffee-related treatments (K/C [1:1], Cafestol-alone, Turkish coffee) …

MaleDNA damageHealth Toxicology and MutagenesisCafestolBiologyCoffeeXenobioticschemistry.chemical_compoundGeneticsmedicineAnimalsDNA Modification MethylasesMolecular BiologyAnticarcinogenCarcinogenKahweolGlutathioneMolecular biologyRatsLiverchemistryBiochemistryDiterpenesAntimutagenDrug metabolismmedicine.drugMutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
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Epigenetic upregulation of endogenous VEGF-A reduces myocardial infarct size in mice.

2014

“Epigenetherapy” alters epigenetic status of the targeted chromatin and modifies expression of the endogenous therapeutic gene. In this study we used lentiviral in vivo delivery of small hairpin RNA (shRNA) into hearts in a murine infarction model. shRNA complementary to the promoter of vascular endothelial growth factor (VEGF-A) was able to upregulate endogenous VEGF-A expression. Histological and multiphoton microscope analysis confirmed the therapeutic effect in the transduced hearts. Magnetic resonance imaging (MRI) showed in vivo that the infarct size was significantly reduced in the treatment group 14 days after the epigenetherapy. Importantly, we show that promoter-targeted shRNA upr…

MaleVascular Endothelial Growth Factor ASmall interfering RNAAnatomy and PhysiologyTranscription GeneticMyocardial InfarctionEndogenyCardiovascularCardiovascular SystemEpigenesis GeneticSmall hairpin RNAMiceMolecular cell biologyNucleic AcidsGene expressionProtein IsoformsRNA Small InterferingCyclic AMP Response Element-Binding ProteinPromoter Regions GeneticRegulation of gene expressionMultidisciplinaryChromosome BiologyQRGenomicsGene TherapyChromatinInterventional CardiologyCell biologyUp-RegulationVascular endothelial growth factor AMedicineEpigeneticsDNA modificationHistone modificationResearch ArticleTranscriptional ActivationDrugs and DevicesScienceDNA transcriptionBiologyDownregulation and upregulationGenomic MedicineGeneticsGene silencingAnimalsGene SilencingBiologyBase SequenceInverted Repeat Sequencesta1182Membrane ProteinsDNA MethylationPhosphoproteinsMolecular biologyMice Inbred C57BLRNAGene expressionPloS one
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“Super p53” Mice Display Retinal Astroglial Changes

2013

Tumour-suppressor genes, such as the p53 gene, produce proteins that inhibit cell division under adverse conditions, as in the case of DNA damage, radiation, hypoxia, or oxidative stress (OS). The p53 gene can arrest proliferation and trigger death by apoptosis subsequent to several factors. In astrocytes, p53 promotes cell-cycle arrest and is involved in oxidative stress-mediated astrocyte cell death. Increasingly, astrocytic p53 is proving fundamental in orchestrating neurodegenerative disease pathogenesis. In terms of ocular disease, p53 may play a role in hypoxia due to ischaemia and may be involved in the retinal response to oxidative stress (OS). We studied the influence of the p53 ge…

PathologyAnatomy and PhysiologyCell divisionMouselcsh:MedicineFluorescent Antibody Techniquemedicine.disease_causechemistry.chemical_compoundMiceMolecular Cell Biologylcsh:ScienceMultidisciplinaryGlial fibrillary acidic proteinAnimal ModelsCell biologymedicine.anatomical_structureMedicineOftalmologíaDNA modificationAstrocyteResearch ArticleSignal TransductionProgrammed cell deathmedicine.medical_specialtyCell PhysiologyHistologyOcular AnatomyNeurocienciasMice TransgenicBiologyRetinaModel OrganismsOcular SystemGlial Fibrillary Acidic ProteinmedicineGeneticsAnimalsBiologyRetinaStaining and Labelinglcsh:RRetinalAnatomía ocularMice Inbred C57BLGenética médicaOphthalmologychemistryApoptosisAstrocytesbiology.proteinlcsh:QGene expressionGene FunctionTumor Suppressor Protein p53Animal GeneticsOxidative stress
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