Search results for " methylation"

showing 10 items of 457 documents

The Binomial “Inflammation-Epigenetics” in Breast Cancer Progression and Bone Metastasis: IL-1β Actions Are Influenced by TET Inhibitor in MCF-7 Cell…

2022

The existence of a tight relationship between inflammation and epigenetics that in primary breast tumor cells can lead to tumor progression and the formation of bone metastases was investigated. It was highlighted how the induction of tumor progression and bone metastasis by Interleukin-1 beta, in a non-metastatic breast cancer cell line, MCF-7, was dependent on the de-methylating actions of ten-eleven translocation proteins (TETs). In fact, the inhibition of their activity by the Bobcat339 molecule, an inhibitor of TET enzymes, determined on the one hand, the modulation of the epithelial-mesenchymal transition process, and on the other hand, the reduction in the expression of markers of bo…

Epithelial-Mesenchymal TransitionDNA methylation; bone metastasis; inflammation; Interleukin-1β; ten-eleven translocation proteins; MCF-7 cell lineInterleukin-1betaBreast NeoplasmsBone NeoplasmsMCF-7 cell lineCatalysisEpigenesis GeneticInorganic ChemistrySettore BIO/13 - Biologia ApplicataCell Line TumorHumansPhysical and Theoretical ChemistryMolecular BiologySpectroscopybone metastasisDNA methylationten-eleven translocation proteinsOrganic ChemistryGeneral MedicineInterleukin-1βComputer Science ApplicationsSettore BIO/18 - GeneticainflammationMCF-7 CellsFemaleInflammatory Breast NeoplasmsInternational Journal of Molecular Sciences
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Gcn5p is involved in the acetylation of histone H3 in nucleosomes.

1997

Abstract Enzymatic extracts from a gcn5 mutant and wild-type strains of Saccharomyces cerevisiae were chromatographically fractionated and the histone acetyltransferase activities compared. When free histones were used as substrate, extracts from wild-type cells showed two peaks of activity on histone H3 but extracts from gcn5 mutant cells showed only one. With nucleosomes as substrate, the histone acetyltransferase activities present in extracts from the gcn5 mutant strain were not able to modify H3 whereas wild-type cell extracts acetylated intensely this histone. The activity that acetylated nucleosome-bound H3 behaved as a 170-kDa complex. We suggest that Gcn5p represents a catalytic su…

ErythrocytesSaccharomyces cerevisiae ProteinsBiophysicsSaccharomyces cerevisiaeBiochemistryFungal ProteinsHistonesHistone H3Histone H1Structural BiologyHistone H2AHistone methylationGeneticsHistone codeAnimalsHistone octamerMolecular BiologyHistone AcetyltransferasesHistone acetyltransferase GCN5biologyAcetylationCell BiologyHistone acetyltransferaseChromatinNucleosomesDNA-Binding ProteinsMolecular WeightBiochemistryNucleosomeHistone methyltransferasebiology.proteinChickensProtein KinasesFEBS letters
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Prevalence of Angelman syndrome and Prader-Willi syndrome in Estonian children: sister syndromes not equally represented.

2006

In 2000-2004, we performed a focused search for individuals with Angelman syndrome (AS) and Prader-Willi syndrome (PWS) aiming to establish the prevalence data for the individuals born between 1984 and 2004 in Estonia. All persons with probable AS or PWS (n = 184) were studied using the DNA methylation test. Individuals with abnormal methylation were all further tested by chromosomal and FISH analysis, and if necessary for uniparental disomy and UBE3A gene mutation. Nineteen cases with abnormal methylation test result were identified. Seven of them had AS, including six (85.7%) due to 15q11-13 deletion and one paternal UPD15. Twelve subjects had PWS: 4 (33%) 15q11-13 deletions, 6 (50%) mate…

EstoniaMalePediatricsmedicine.medical_specialtyPopulationDNA Mutational AnalysisPrevalenceChromosomal translocationAngelman syndromeInternal medicineEpidemiologyHappy puppet syndromeGeneticsmedicinePrevalenceHumanseducationChildGenetics (clinical)In Situ Hybridization Fluorescenceeducation.field_of_studyMolecular Epidemiologybusiness.industryDNA Methylationmedicine.diseaseUniparental disomyChromosome BandingEndocrinologyEl NiñoFemaleAngelman SyndromebusinessPrader-Willi SyndromeAmerican journal of medical genetics. Part A
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De novo SMARCA2 variants clustered outside the helicase domain cause a new recognizable syndrome with intellectual disability and blepharophimosis di…

2020

International audience; Purpose: Nontruncating variants in SMARCA2, encoding a catalytic subunit of SWI/SNF chromatin remodeling complex, cause Nicolaides-Baraitser syndrome (NCBRS), a condition with intellectual disability and multiple congenital anomalies. Other disorders due to SMARCA2 are unknown.Methods: By next-generation sequencing, we identified candidate variants in SMARCA2 in 20 individuals from 18 families with a syndromic neurodevelopmental disorder not consistent with NCBRS. To stratify variant interpretation, we functionally analyzed SMARCA2 variants in yeasts and performed transcriptomic and genome methylation analyses on blood leukocytes.Results: Of 20 individuals, 14 showed…

Foot DeformitiesFoot Deformities Congenital[SDV]Life Sciences [q-bio]BiologyBlepharophimosisSettore MED/03 - GENETICA MEDICAHypotrichosisChromatin remodeling03 medical and health sciencesCongenital0302 clinical medicineNeurodevelopmental disorderIntellectual DisabilityIntellectual disabilitySMARCA2medicineHumansGeneGenetics (clinical)030304 developmental biologyGenetics0303 health sciencesBISFaciesmedicine.diseaseBlepharophimosisPhenotypeneurodevelopmental disorderPhenotypeNicolaides–Baraitser syndromeintellectual disabilityDNA methylationNicolaides–Baraitser syndrome030217 neurology & neurosurgeryTranscription FactorsGenetics in medicine : official journal of the American College of Medical Genetics
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GADD45a physically and functionally interacts with TET1

2015

AbstractDNA demethylation plays a central role during development and in adult physiology. Different mechanisms of active DNA demethylation have been established. For example, Growth Arrest and DNA Damage 45-(GADD45) and Ten-Eleven-Translocation (TET) proteins act in active DNA demethylation but their functional relationship is unresolved. Here we show that GADD45a physically interacts – and functionally cooperates with TET1 in methylcytosine (mC) processing. In reporter demethylation GADD45a requires endogenous TET1 and conversely TET1 requires GADD45a. On GADD45a target genes TET1 hyperinduces 5-hydroxymethylcytosine (hmC) in the presence of GADD45a, while 5-formyl-(fC) and 5-carboxylcyto…

Gadd45Cancer ResearchDNA damageCell Cycle ProteinsBiologyDNA-binding proteinArticleMixed Function OxygenaseshmCchemistry.chemical_compoundCytosineLC–MS/MSProto-Oncogene ProteinsHumansImmunoprecipitationMolecular BiologyDemethylationGadd45Nuclear ProteinsOxidative DNA demethylationCell BiologyDNA MethylationDNA-Binding Proteins5-MethylcytosineDNA demethylationHEK293 CellschemistryBiochemistryGene Knockdown TechniquesDNA methylationDNA demethylation5-MethylcytosineOxidation-ReductionTETProtein BindingDevelopmental BiologyDifferentiation
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miR-486-5p expression is regulated by DNA methylation in osteosarcoma.

2022

Abstract Background Osteosarcoma is the most common primary malignant tumour of bone occurring in children and young adolescents and is characterised by complex genetic and epigenetic changes. The miRNA miR-486-5p has been shown to be downregulated in osteosarcoma and in cancer in general. Results To investigate if the mir-486 locus is epigenetically regulated, we integrated DNA methylation and miR-486-5p expression data using cohorts of osteosarcoma cell lines and patient samples. A CpG island in the promoter of the ANK1 host gene of mir-486 was shown to be highly methylated in osteosarcoma cell lines as determined by methylation-specific PCR and direct bisulfite sequencing. High methylati…

Gene Expression Regulation NeoplasticMicroRNAsOsteosarcomaCell Line TumorGeneticsHumansBone NeoplasmsDNA MethylationBiotechnologyCell ProliferationEpigenesis GeneticBMC genomics
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Epigenetic modifiers are necessary but not sufficient for reprogramming non-myelinating cells into myelin gene-expressing cells.

2010

Background Modifications on specific histone residues and DNA methylation play an essential role in lineage choice and cellular reprogramming. We have previously shown that histone modifications or combinatorial codes of transcription factors (TFs) are critical for the differentiation of multipotential progenitors into myelinating oligodendrocytes. In this study we asked whether combining global manipulation of DNA methylation and histone acetylation together with the expression of oligodendrocyte- specific TFs, was sufficient to switch the identity of fibroblasts into myelin gene-expressing cells. Methodology/Principal Findings Transfection of six oligodendrocyte-specific TFs (Olig1, Olig2…

Gene Expressionlcsh:MedicineBiologyCell LineEpigenesis GeneticHistones03 medical and health sciencesMice0302 clinical medicineHistone H1Histone methylationHistone H2ANeuroscience/Neuronal Signaling MechanismsHistone codeAnimalsCell Lineagelcsh:ScienceCells Cultured030304 developmental biologyEpigenomics0303 health sciencesMultidisciplinaryNeuroscience/Neuronal and Glial Cell BiologyMultipotent Stem Cellslcsh:RAcetylationCell DifferentiationDNA MethylationFibroblastsMolecular biologyChromatinChromatinRatsOligodendrogliaHomeobox Protein Nkx-2.2Histone methyltransferaseNIH 3T3 Cellslcsh:QNeuroscience/Neurobiology of Disease and RegenerationChromatin immunoprecipitation030217 neurology & neurosurgeryMyelin ProteinsResearch ArticleNeuroscienceTranscription FactorsPLoS ONE
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Autoregulation of NFATc1/A Expression Facilitates Effector T Cells to Escape from Rapid Apoptosis

2002

AbstractThreshold levels of individual NFAT factors appear to be critical for apoptosis induction in effector T cells. In these cells, the short isoform A of NFATc1 is induced to high levels due to the autoregulation of the NFATc1 promoter P1 by NFATs. P1 is located within a CpG island in front of exon 1, represents a DNase I hypersensitive chromatin site, and harbors several sites for binding of inducible transcription factors, including a tandemly arranged NFAT site. A second promoter, P2, before exon 2, is not controlled by NFATs and directs synthesis of the longer NFATc1/B+C isoforms. Contrary to other NFATs, NFATc1/A is unable to promote apoptosis, suggesting that NFATc1/A enhances eff…

Gene isoformTranscription GeneticMolecular Sequence DataImmunologyApoptosisBiologyT-Lymphocytes RegulatoryJurkat CellsMiceExonAnimalsDeoxyribonuclease IHomeostasisHumansImmunology and AllergyPromoter Regions GeneticTranscription factorMice Inbred BALB CBase SequenceNFATC Transcription Factorsintegumentary systemEffectorNuclear ProteinsNFATDNA MethylationMolecular biologyChromatinDNA-Binding ProteinsAlternative SplicingInfectious DiseasesCpG siteApoptosisElectrophoresis Polyacrylamide GelPoly ATranscription FactorsImmunity
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PTHrP in differentiating human mesenchymal stem cells: Transcript isoform expression, promoter methylation, and protein accumulation

2013

Human PTHrP gene displays a complex organization with nine exons producing diverse mRNA variants due to alternative splicing at 5' and 3' ends and the existence of three different transcriptional promoters (P1, P2 and P3), two of which (P2 and P3) contain CpG islands. It is known that the expression of PTHrP isoforms may be differentially regulated in a developmental stage- and tissue-specific manner. To search for novel molecular markers of stemness/differentiation, here we have examined isoform expression in fat-derived mesenchymal stem cells both maintained in stem conditions and induced toward adipo- and osteogenesis. In addition, the expression of the splicing isoforms derived from P2 …

Gene isoformTranscription GeneticPTHrPCellular differentiationpromoter methylationBiologyOsteocytesBiochemistryGene expressionAdipocytesHumansProtein IsoformsadipogenesiSettore BIO/06 - Anatomia Comparata E CitologiaPromoter Regions Geneticmesenchymal stem cellCells CulturedMessenger RNAMesenchymal stem cellAlternative splicingParathyroid Hormone-Related ProteinCell DifferentiationMesenchymal Stem CellsExonsGeneral MedicineMethylationDNA MethylationosteogenesiMolecular biologyIntronsPTHrP; mesenchymal stem cells; osteogenesis; adipogenesis; gene expression; promoter methylationAlternative SplicingSettore BIO/18 - GeneticaGene Expression Regulationgene expressionCpG IslandsStem cellBiochimie
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Epigenetic biomarkers: Current strategies and future challenges for their use in the clinical laboratory

2017

Epigenetic modifications and regulators represent potential molecular elements which control relevant physiological and pathological features, thereby contributing to the natural history of human disease. These epigenetic modulators can be employed as disease biomarkers, since they show several advantages and provide information about gene function, thus explaining differences among patient endophenotypes. In addition, epigenetic biomarkers can incorporate information regarding the effects of the environment and lifestyle on health and disease, and monitor the effect of applied therapies. Technologies used to analyze these epigenetic biomarkers are constantly improving, becoming much easier…

Genetic Markers0301 basic medicineEpigenetic biomarkersComputer scienceBiochemistry (medical)Clinical BiochemistryGenomicsGenomicsDiseaseDNA MethylationPrecision medicineClinical routineArticleGeneral Biochemistry Genetics and Molecular BiologyEpigenesis Genetic03 medical and health sciences030104 developmental biologyMolecular Diagnostic TechniquesRisk analysis (engineering)HumansBiomarker (medicine)Disease biomarkerEpigeneticsCritical Reviews in Clinical Laboratory Sciences
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