Search results for "Histone Methyltransferases"

showing 4 items of 4 documents

Drosophila Enhancer of Zeste/ESC Complexes Have a Histone H3 Methyltransferase Activity that Marks Chromosomal Polycomb Sites

2002

AbstractEnhancer of Zeste is a Polycomb Group protein essential for the establishment and maintenance of repression of homeotic and other genes. In the early embryo it is found in a complex that includes ESC and is recruited to Polycomb Response Elements. We show that this complex contains a methyltransferase activity that methylates lysine 9 and lysine 27 of histone H3, but the activity is lost when the E(Z) SET domain is mutated. The lysine 9 position is trimethylated and this mark is closely associated with Polycomb binding sites on polytene chromosomes but is also found in centric heterochromatin, chromosome 4, and telomeric sites. Histone H3 methylated in vitro by the E(Z)/ESC complex …

Histone methyltransferase activitygovernment.form_of_governmentSettore BIO/11 - Biologia Molecolaremacromolecular substancesTrithorax-group proteinsGeneral Biochemistry Genetics and Molecular BiologyChromosomesHistone H3SUZ12AnimalsDrosophila ProteinsPRC1 complexProtein MethyltransferasesMethyltransferasePolycomb Repressive Complex 1biologyBiochemistry Genetics and Molecular Biology(all)Histone H3LysinefungiPolycomb Repressive Complex 2Nuclear ProteinsHistone-Lysine N-MethyltransferaseMethyltransferasesMolecular biologyPolycombRepressor ProteinsMutationgovernmentbiology.proteinHistone MethyltransferasesDrosophilaHomeotic genePRC2Centric heterochromatinProtein BindingCell
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3-Deazaneplanocin A (DZNep), an Inhibitor of the Histone Methyltransferase EZH2, Induces Apoptosis and Reduces Cell Migration in Chondrosarcoma Cells

2014

Objective Growing evidences indicate that the histone methyltransferase EZH2 (enhancer of zeste homolog 2) may be an appropriate therapeutic target in some tumors. Indeed, a high expression of EZH2 is correlated with poor prognosis and metastasis in many cancers. In addition, 3-Deazaneplanocin A (DZNep), an S-adenosyl-L homocysteine hydrolase inhibitor which induces EZH2 protein depletion, leads to cell death in several cancers and tumors. The aim of this study was to determine whether an epigenetic therapy targeting EZH2 with DZNep may be also efficient to treat chondrosarcomas. Methods EZH2 expression was determined by immunohistochemistry and western-blot. Chondrosarcoma cell line CH2879…

MESH: Cell DeathAdenosine[SDV]Life Sciences [q-bio]Cancer Treatmentlcsh:MedicineMESH: Flow CytometryApoptosischemistry.chemical_compoundSpectrum Analysis Techniques0302 clinical medicineCell MovementMolecular Cell BiologyMedicine and Health Sciences3-Deazaneplanocin AMESH: Epigenesis GeneticEnzyme Inhibitorslcsh:Science0303 health sciencesMultidisciplinaryCell DeathbiologyReverse Transcriptase Polymerase Chain ReactionEZH2Polycomb Repressive Complex 2DrugsCell migrationMESH: ChondrosarcomaFlow Cytometry3. Good healthHistone[SDV.MHEP.RSOA]Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal systemOncologyConnective TissueCell ProcessesSpectrophotometry030220 oncology & carcinogenesisHistone methyltransferaseHistone MethyltransferasesMESH: 3-deazaneplanocinCytophotometryAnatomyMESH: Polycomb Repressive Complex 2Epigenetic therapyMESH: Histone methyltransferaseResearch ArticleProgrammed cell deathHistologyChondrosarcoma[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular Biologymacromolecular substancesResearch and Analysis MethodsCell GrowthEpigenetic Therapy03 medical and health sciencesRheumatologyCell Line TumorMESH: Blotting WesternHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyEZH2Tumors030304 developmental biologyMESH: Apoptosislcsh:RMESH: Histone-Lysine N-MethyltransferaseBiology and Life SciencesMESH: ImmunohistochemistryHistone-Lysine N-MethyltransferaseCell BiologyBiological TissueCartilageHistone methyltransferasechemistryApoptosisbiology.proteinCancer researchMESH: EZH2 protein humanlcsh:QCytometry
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Chromatin dynamics of the developmentally regulated P. lividus neural alpha tubulin gene

2011

Over 40 years ago, Allfrey and colleagues (1964) suggested that two histone modifications, namely acetylation and methylation, might regulate RNA synthesis. Nowadays it is universally accepted that activation of gene expression strictly depends on enzymatic mechanisms able to dynamically modify chromatin structure. Here, using techniques including DNaseI hypersensitive site analysis, chomatin immunoprecipitation and quantitative PCR analysis, we have analyzed the dynamics of histone post-translation modifications involved in developmentally/spatially controlled activation of the sea urchin PlTalpha2 tubulin gene. We have demonstrated that only when the PlTalpha2 core promoter chromatin is a…

Chromatin ImmunoprecipitationEmbryologyRNA polymerase IISettore BIO/11 - Biologia MolecolareMethylationNervous SystemHistone DeacetylasesHistonesTubulinGene expressionAnimalsParacentrotus lividus chromatin modification epigenetic reprogramming nervous systemPromoter Regions GeneticHistone AcetyltransferasesEpigenomicsHistone DemethylasesbiologyGene Expression Regulation DevelopmentalAcetylationPromoterHistone-Lysine N-MethyltransferaseMolecular biologyChromatinChromatinCell biologyHistoneAcetylationHistone MethyltransferasesParacentrotusbiology.proteinRNA Polymerase IIProtein Processing Post-TranslationalHypersensitive siteDevelopmental Biology
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Familial Sotos syndrome caused by a novel missense mutation, C2175S, in NSD1 and associated with normal intelligence, insulin dependent diabetes, bro…

2009

We report a familial Sotos syndrome in two children, boy and girl, aged 17 and 8 years, and in their 44 year old mother, who displayed normal intelligence at adult age, but suffered from insulin dependent diabetes mellitus, bronchial asthma, and severe lipedema. The underlying missense mutation, C2175S, occurred in a conserved segment of the NSD1 gene. Our findings confirm that familial cases of SS are more likely to carry missense mutations. This case report may prove useful to avoid underestimation of the recurrence rate of SS, and to demonstrate that the developmental delay may normalize, enabling an independent life and having an own family.

AdultMalemedicine.medical_specialtyPediatricsAdolescentLipid Metabolism DisordersMutation MissenseGermanyInternal medicineImmunopathologyGeneticsHumansMedicineMissense mutationGrowth DisordersGenetics (clinical)AsthmaAutoimmune diseaseType 1 diabetesbusiness.industrySotos syndromeRespiratory diseaseIntracellular Signaling Peptides and ProteinsLipoedemaNuclear ProteinsHistone-Lysine N-MethyltransferaseSyndromeGeneral Medicinemedicine.diseaseAsthmaDiabetes Mellitus Type 1EndocrinologyHistone MethyltransferasesFemalebusinessEuropean Journal of Medical Genetics
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