2024
PRMT6 facilitates EZH2 protein stability by inhibiting TRAF6-mediated ubiquitination degradation to promote glioblastoma cell invasion and migration
Wang J, Shen S, You J, Wang Z, Li Y, Chen Y, Tuo Y, Chen D, Yu H, Zhang J, Wang F, Pang X, Xiao Z, Lan Q, Wang Y. PRMT6 facilitates EZH2 protein stability by inhibiting TRAF6-mediated ubiquitination degradation to promote glioblastoma cell invasion and migration. Cell Death & Disease 2024, 15: 524. PMID: 39043634, PMCID: PMC11266590, DOI: 10.1038/s41419-024-06920-2.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBrain NeoplasmsCell Line, TumorCell MovementEnhancer of Zeste Homolog 2 ProteinFemaleGene Expression Regulation, NeoplasticGlioblastomaHumansMaleMiceMice, Inbred BALB CMice, NudeNeoplasm InvasivenessNuclear ProteinsProtein StabilityProtein-Arginine N-MethyltransferasesProteolysisTNF Receptor-Associated Factor 6UbiquitinationConceptsProtein arginine methyltransferase 6Glioblastoma cell invasionStability of EZH2Protein stabilityCell invasionOverexpression of PRMT6Inhibited glioblastoma cell invasionGlioblastoma cellsEZH2 protein stabilityHistone methylation marksMigration of glioblastoma cellsHallmarks of cancerProliferation of glioblastoma cellsMethylation marksTumor cell invasionEpigenetic regulationGlioblastoma cells in vivoBioinformatics analysisMigration in vitroRegulatory relationshipsEZH2 proteinUbiquitination degradationProteinCells in vivoTRAF6
2023
KDM5 Lysine Demethylases in Pathogenesis, from Basic Science Discovery to the Clinic
Zhang S, Cao J, Yan Q. KDM5 Lysine Demethylases in Pathogenesis, from Basic Science Discovery to the Clinic. Advances In Experimental Medicine And Biology 2023, 1433: 113-137. PMID: 37751138, DOI: 10.1007/978-3-031-38176-8_6.ChaptersConceptsPlant homeodomainFamily proteinsKey epigenetic markCell fate determinationHistone methylation marksCancer type-dependent mannerKetoglutarate-dependent dioxygenasesSelective KDM5 inhibitorsTumor suppressive functionType-dependent mannerEpigenetic marksTumor suppressive roleFate determinationJumonji CLysine 4Active chromatinMethylation marksHistone H3Lysine demethylasesCatalytic coreKDM5 inhibitorsDrug targetsKDM5Cancer metastasisSuppressive role
2014
Relationship of DNA Methylation and Gene Expression in Idiopathic Pulmonary Fibrosis
Yang IV, Pedersen BS, Rabinovich E, Hennessy CE, Davidson EJ, Murphy E, Guardela BJ, Tedrow JR, Zhang Y, Singh MK, Correll M, Schwarz MI, Geraci M, Sciurba FC, Quackenbush J, Spira A, Kaminski N, Schwartz DA. Relationship of DNA Methylation and Gene Expression in Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2014, 190: 1263-1272. PMID: 25333685, PMCID: PMC4315819, DOI: 10.1164/rccm.201408-1452oc.Peer-Reviewed Original ResearchConceptsGene expressionDNA methylationMethylation marksMethylation changesQuantitative trait lociTrans-gene expressionIntegrative genomic analysisTrait lociEpigenetic mechanismsTranscriptional changesGenomic analysisTranscription factorsCASZ1 expressionTarget genesFunctional validationExpression relationshipsMethylationGenesDMRsExpressionEnvironmental factorsTargeted analysisPathogenesis of IPFComplex interactionsTranscriptome
2002
BORIS, a novel male germ-line-specific protein associated with epigenetic reprogramming events, shares the same 11-zinc-finger domain with CTCF, the insulator protein involved in reading imprinting marks in the soma
Loukinov DI, Pugacheva E, Vatolin S, Pack SD, Moon H, Chernukhin I, Mannan P, Larsson E, Kanduri C, Vostrov AA, Cui H, Niemitz EL, Rasko JE, Docquier FM, Kistler M, Breen JJ, Zhuang Z, Quitschke WW, Renkawitz R, Klenova EM, Feinberg AP, Ohlsson R, Morse HC, Lobanenkov VV. BORIS, a novel male germ-line-specific protein associated with epigenetic reprogramming events, shares the same 11-zinc-finger domain with CTCF, the insulator protein involved in reading imprinting marks in the soma. Proceedings Of The National Academy Of Sciences Of The United States Of America 2002, 99: 6806-6811. PMID: 12011441, PMCID: PMC124484, DOI: 10.1073/pnas.092123699.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsCCCTC-Binding FactorCloning, MolecularDNA MethylationDNA-Binding ProteinsGene ExpressionGenetic MarkersGenomic ImprintingHumansMaleMiceMolecular Sequence DataProtein Structure, TertiaryRepressor ProteinsSequence Homology, Amino AcidTestisTranscription FactorsZinc FingersConceptsMethylation marksSame DNA-binding domainMale germ cell developmentMale germ line developmentEpigenetic reprogramming eventsGerm line developmentDNA-binding domainDNA-binding potentialMale germ lineGerm cell developmentX-chromosome inactivationMethylation-sensitive insulatorInsulator proteinsParalogous genesDistinct aminoReprogramming eventsImprinting marksGene regulationChromosome inactivationGerm lineCTCF geneCTCF expressionCarboxy terminusCTCFCandidate proteins
2001
Accelerated age-related CpG island methylation in ulcerative colitis.
Issa JP, Ahuja N, Toyota M, Bronner MP, Brentnall TA. Accelerated age-related CpG island methylation in ulcerative colitis. Cancer Research 2001, 61: 3573-7. PMID: 11325821.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAdultAge FactorsAgedCarrier ProteinsChondroitin Sulfate ProteoglycansColitis, UlcerativeColonic NeoplasmsCpG IslandsDNA MethylationGenes, p16HumansIntestinal MucosaLectins, C-TypeMiddle AgedMutL Protein Homolog 1MyoD ProteinNeoplasm ProteinsNuclear ProteinsPrecancerous ConditionsReceptors, EstrogenVersicansConceptsMechanism of geneP16 exon 1Exon 1CpG island hypermethylationCpG island methylationMethylation marksMethylation patternsUndesirable genesColorectal epithelial cellsIsland hypermethylationIsland methylationGenesMethylationPremature agingMyoDColon cancerHigh-grade dysplasiaEpithelial cellsCell turnoverHypermethylationNon-UC controlsNormal appearing epitheliumUlcerative colitisHigh levelsCSPG2
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