Search results for "Methylation"

showing 10 items of 607 documents

IL-1b induces DNA demethylation, at genome level and in specific CpG sites of IL-6 and IL-8 genes in human intestinal epithelial cells

2015

Inflammation is a complex physiological response that requires the activity of a sophisticated regulatory network involving the activation of specific genes for defense, tissue repair and remodeling. Although transcriptional activation has been shown to be critical in the regulation of inflammatory genes (1) the role of epigenetic phenomena in the modulation of the inflammatory response is now emerging (2). Specifically, it has been recently reported that proinflammatory stimuli induce DNA demethylation in the interleukin IL-1 promoter of human articular chondrocytes (3). IL-1 cytokine, among several proinflammatory agents, represents an essential player in the inflammatory conditions of …

IL1-b DNA Methylation EpigeneticsSettore BIO/18 - GeneticaSettore BIO/10 - Biochimica
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DNA Methylation and Non-Coding RNAs during Tissue-Injury Associated Pain.

2022

While about half of the population experience persistent pain associated with tissue damages during their lifetime, current symptom-based approaches often fail to reduce such pain to a satisfactory level. To provide better patient care, mechanism-based analgesic approaches must be developed, which necessitates a comprehensive understanding of the nociceptive mechanism leading to tissue injury-associated persistent pain. Epigenetic events leading the altered transcription in the nervous system are pivotal in the maintenance of pain in tissue injury. However, the mechanisms through which those events contribute to the persistence of pain are not fully understood. This review provides a summar…

INFLAMMATORY PAINRNA UntranslatedChemistry MultidisciplinaryAdaptation BiologicalReviewUP-REGULATIONEpigenesis GeneticCpG islandsTranscripció genèticalncRNANeurociènciesnociceptionBiology (General)SpectroscopyGENE-EXPRESSIONGeneral MedicineComputer Science ApplicationsChemistryPhysical SciencesDisease SusceptibilityChronic PainLife Sciences & BiomedicineepigeneticALLEVIATES NEUROPATHIC PAINBiochemistry & Molecular Biologydorsal root ganglionQH301-705.50699 Other Biological SciencesCatalysisCONTRIBUTESInorganic ChemistryDiagnosis DifferentialCENTRAL SENSITIZATION0399 Other Chemical SciencesHumansPhysical and Theoretical ChemistryQD1-999Molecular Biologyspinal dorsal hornmiRNACHRONIC CONSTRICTION INJURYneuropathic pain0604 GeneticsScience & TechnologyChemical PhysicsNERVE INJURYMICRORNAGene Expression ProfilingOrganic ChemistryDNA MethylationCPG-BINDING PROTEIN-2gene transcriptionGene Expression RegulationsiRNARNAWounds and InjuriesBiomarkersInternational journal of molecular sciences
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Comparative study on the inhibition of Na+, K+-activated ATPase activity by chlorpromazine, promazine, imipramine, and their monodesmethyl metabolites

1972

The inhibition of the sodium- and potassium-activated adenosine triphosphatase (Na-K-ATPase, EC 3.6.1.3) activity by chlorpromazine, promazine and imipramine was compared with that by the monodesmethyl metabolites of these drugs. The experiments were performed with a deoxycholate- and sodium iodide-treated microsomal enzyme preparation from rat brain. It was shown in dose-response curves as well as in double-reciprocal Lineweaver-Burk plots of Na-K-ATPase activity against KCl concentration that the monodesmethyl metabolites were stronger inhibitors than their parent compounds. The results obtained with the desmethyl metabolites and imipramine as inhibitors indicate competitive inhibition wh…

ImipramineChlorpromazineReceptors DrugSodiumchemistry.chemical_elementPharmacologyMethylationImipramineNon-competitive inhibitionMicrosomesDesipraminemedicineAnimalsChlorpromazinePromazinePromazineAdenosine TriphosphatasesPharmacologychemistry.chemical_classificationChemistrySodiumBrainGeneral MedicineDesmethylRatsEnzyme ActivationBiochemistryPotassiumFemaleProtein Bindingmedicine.drugTricyclicNaunyn-Schmiedeberg's Archives of Pharmacology
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Expression profiling of autoimmune regulator AIRE mRNA in a comprehensive set of human normal and neoplastic tissues.

2006

Defects in the autoimmune regulator (AIRE) gene cause the monogenic autoimmune disease autoimmune polyendocrinopathy syndrome type 1 (APS-1), which is characterized by a loss of self-tolerance to multiple organs. In concordance with its role in immune tolerance, AIRE is strongly expressed in medullary thymic epithelial cells (mTECs). Data on mechanisms controlling AIRE activation and the expression of this gene in other tissues are fragmentary and controversial. We report here AIRE mRNA expression profiling of a large set of normal human tissues and cells, tumor specimen and methylation deficient cell lines. On this broad data basis we found that AIRE mRNA expression is confined to mTECs in…

Immune Tolerance/geneticsThymus Gland/immunologyTranscription GeneticImmunologyTranscription Genetic/immunologyThymus GlandBiologyLymph Nodes/immunologymedicine.disease_causeAutoimmunityImmune toleranceCell Line TumorNeoplasmsmedicineTranscriptional regulationImmune ToleranceImmunology and AllergyHumansRNA MessengerPolyendocrinopathies AutoimmuneGeneTranscription Factors/biosynthesisAutoimmune diseaseReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingRNA Messenger/biosynthesisDNA Methylationmedicine.diseaseAutoimmune regulatorNeoplasms/geneticsPolyendocrinopathies Autoimmune/geneticsGene expression profilingGene Expression Regulation NeoplasticDNA methylationImmunologyCancer researchLymph NodesGene Expression Profiling/methodsTranscription FactorsImmunology letters
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A novel high-spin heterometallic Ni12K4cluster incorporating large Ni–azide circles and an in situ cyanomethylated di-2-pyridyl ketone

2005

Reaction of di-2-pyridyl ketone (dpk) with nickel acetate and azide in the presence of potassium tert-butylate as a catalytic base generates the title compound, which contains the largest [Ni(m1,1-N3)]6 circles in the discrete ferromagnetically-coupled MII–azide cluster family, and shows an unprecedented in situ cyanomethylation of ketone. Clemente Juan, Juan Modesto, Juan.M.Clemente@uv.es

In situPotassium tert-butylateKetoneBase (chemistry)UNESCO::QUÍMICAPotassiumchemistry.chemical_elementCyanomethylation of ketone:QUÍMICA [UNESCO]Ferromagnetically-coupled Mll-azideCatalysisCatalysischemistry.chemical_compoundPolymer chemistryMaterials ChemistryCluster (physics)Organic chemistrySpin (physics)Novelchemistry.chemical_classificationUNESCO::QUÍMICA::Química inorgánicaMetals and AlloysNickel acetateGeneral Chemistry:QUÍMICA::Química inorgánica [UNESCO]Cyanomethylation of ketone ; Potassium tert-butylate ; Ferromagnetically-coupled Mll-azide ; Nickel acetate ; NovelSurfaces Coatings and FilmsElectronic Optical and Magnetic MaterialschemistryCeramics and CompositesAzideChem. Commun.
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3-[4-(1H-indol-3-yl)-1,3-thiazol-2-yl]-1H-pyrrolo[2,3-b]pyridines, nortopsentin Analogues with antiproliferative activity

2015

A new series of nortopsentin analogues, in which the imidazole ring of the natural product was replaced by thiazole and the indole unit bound to position 2 of the thiazole ring was substituted by a 7-azaindole moiety, was efficiently synthesized. Two of the new nortopsentin analogues showed good antiproliferative effect against the totality of the NCI full panel of human tumor cell lines (~60) having GI50 values ranging from low micromolar to nanomolar level. The mechanism of the antiproliferative effect of these derivatives, investigated on human hepatoma HepG2 cells, was pro-apoptotic, being associated with externalization of plasma membrane phosphatidylserine and mitochondrial dysfunctio…

IndolesHalogenationPyridines3-b]pyridinesPharmaceutical ScienceApoptosisAntiproliferative activity3-[4-(1<i>H</i>-indol-3-yl)-13-thiazol-2-yl]-1<i>H</i>-pyrrolo[23-<i>b</i>]pyridineschemistry.chemical_compoundNeoplasmsDrug DiscoveryImidazoleMoietyindolyl alkaloidsPharmacology Toxicology and Pharmaceutics (miscellaneous)lcsh:QH301-705.5Membrane Potential MitochondrialMolecular Structure3-[4-(1H-indol-3-yl)-1; 3-thiazol-2-yl]-1H-pyrrolo[2; 3-b]pyridines; Antiproliferative activity; Indolyl alkaloids; Marine alkaloids; Nortopsentin analogues; Drug Discovery3003 Pharmaceutical ScienceImidazolesPhosphatidylserineMitochondrianortopsentin analoguesIndolyl alkaloidmarine alkaloidsG2 PhaseStereochemistryNortopsentin analogueAntineoplastic AgentsMethylationResting Phase Cell CycleArticleAlkaloids3-[4-(1H-indol-3-yl)-1Cell Line TumorHumansPyrroles3-[4-(1H-indol-3-yl)-13-thiazol-2-yl]-1H-pyrrolo[23-b]pyridines3-thiazol-2-yl]-1H-pyrrolo[2ThiazoleCell ProliferationIndole testNatural productCell growthDrug Discovery3003 Pharmaceutical ScienceSettore CHIM/08 - Chimica FarmaceuticaThiazoleschemistrylcsh:Biology (General)Cell cultureDrug DesignMarine alkaloid3-[4-(1H-indol-3-yl)-13-thiazol-2-yl]-1H-pyrrolo[23-b]pyridine
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Induced Pluripotent Mesenchymal Stromal Cell Clones Retain Donor-derived Differences in DNA Methylation Profiles

2012

Reprogramming of somatic cells into induced pluripotent stem cells (iPSCs) is an epigenetic phenomenon. It has been suggested that iPSC retain some tissue-specific memory whereas little is known about interindividual epigenetic variation. We have reprogrammed mesenchymal stromal cells from human bone marrow (iP-MSC) and compared their DNA methylation profiles with initial MSC and embryonic stem cells (ESCs) using high-density DNA methylation arrays covering more than 450,000 CpG sites. Overall, DNA methylation patterns of iP-MSC and ESC were similar whereas some CpG sites revealed highly significant differences, which were not related to parental MSC. Furthermore, hypermethylation in iP-MSC…

Induced Pluripotent Stem CellsBiologyDrug DiscoveryGeneticsHumansEpigeneticsCancer epigeneticsInduced pluripotent stem cellMolecular BiologyPharmacologyMesenchymal Stromal CellsReverse Transcriptase Polymerase Chain ReactionMesenchymal Stem CellsMethylationDNA MethylationFlow CytometryMolecular biologyEmbryonic stem cellImmunohistochemistryClone CellsCpG siteDNA methylationMolecular MedicineOriginal ArticleCpG IslandsReprogrammingMolecular Therapy
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Reproductive medicine and inheritance of infertility by offspring: the role of fetal programming.

2011

Objective To summarize the molecular processes involved in fetal programming, to describe how assisted reproduction technologies (ART) may affect the epigenetic pattern of the embryo, and to highlight the current knowledge of the role of perinatal events in the subsequent development of reproductive pathology affecting infertile patients. Design A literature review of fetal programming of adulthood gynecologic diseases and ART. A Medline search was performed with the following keywords: (fetal programming OR epigenetics OR methylation OR acetylation) AND (IVF OR ART) AND (gynecology). Articles up to October 2010 were selected. Articles and recent reviews were classified by human and animals…

Infertilitymedicine.medical_specialtyOffspringPopulationMEDLINEReproductive medicineBioinformaticsEpigenesis GeneticPregnancymedicineHumansEpigeneticseducationGynecologyeducation.field_of_studyFetusbusiness.industryObstetrics and GynecologyDNA Methylationmedicine.diseaseReproductive MedicinePrenatal Exposure Delayed EffectsObservational studyFemalebusinessGenital Diseases FemaleInfertility FemaleFertility and sterility
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Ovulation induction and epigenetic anomalies

2013

In this systematic review of ovulation induction and epigenetic control, studies mainly done in the mouse model highlight how hormone treatments may be prejudicial to the epigenetic reprogramming of gametes as well as early embryos. Moreover, the hormone protocols used in assisted reproduction may also modify the physiologic environment of the uterus, a potential link to endometrial epigenetic disturbances. At present, the few available data in humans are insufficient to allow us to independently determine the impact of a woman's age and infertility problems and treatment protocols and hormone doses on such processes as genomic imprinting.

Infertilitymedicine.medical_specialtyReproductive Techniques Assistedmedicine.medical_treatmentBiologyBioinformaticsEpigenesis GeneticMiceOvulation InductionInternal medicinemedicineAnimalsHumansEpigeneticsEpigenesisGenetic Diseases InbornObstetrics and Gynecologymedicine.diseaseEndocrinologyReproductive MedicineModels AnimalDNA methylationFemaleOvulation inductionGenomic imprintingReprogrammingHormoneFertility and Sterility
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Methylation and Demethylation in Cobaltabis(dicarbollide) Derivatives

2003

B(8)−R and B(8‘)−R (R = alkyl) disubstituted derivatives of the cobaltabis(dicarbollide) anion [3,3‘-Co(C2B9H11)2]- are reported. The synthesis was achieved by application of a modified Kumada reac...

Inorganic Chemistrychemistry.chemical_classificationchemistryStereochemistryOrganic ChemistryMethylationPhysical and Theoretical ChemistryAlkylDemethylationOrganometallics
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