2016
Targeting the histone methyltransferase G9a activates imprinted genes and improves survival of a mouse model of Prader–Willi syndrome
Kim Y, Lee HM, Xiong Y, Sciaky N, Hulbert SW, Cao X, Everitt JI, Jin J, Roth BL, Jiang YH. Targeting the histone methyltransferase G9a activates imprinted genes and improves survival of a mouse model of Prader–Willi syndrome. Nature Medicine 2016, 23: 213-222. PMID: 28024084, PMCID: PMC5589073, DOI: 10.1038/nm.4257.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlotting, WesternCell LineDisease Models, AnimalEnzyme InhibitorsEpigenesis, GeneticFemaleFibroblastsGene ExpressionGenomic ImprintingHistone CodeHistone-Lysine N-MethyltransferaseHumansImmunohistochemistryMaleMethylationMicePrader-Willi SyndromeQuinazolinesReverse Transcriptase Polymerase Chain ReactionRNA, Small NucleolarSnRNP Core ProteinsSurvival RateUbiquitin-Protein Ligases
2011
E6AP is required for replicative and oncogene-induced senescence in mouse embryo fibroblasts
Levav-Cohen Y, Wolyniec K, Alsheich-Bartok O, Chan A, Woods S, Jiang Y, Haupt S, Haupt Y. E6AP is required for replicative and oncogene-induced senescence in mouse embryo fibroblasts. Oncogene 2011, 31: 2199-2209. PMID: 21927031, DOI: 10.1038/onc.2011.402.Peer-Reviewed Original ResearchConceptsMouse embryo fibroblastsOncogene-induced senescenceCellular responsesEmbryo fibroblastsCellular stress responseRas-induced senescenceE3 ubiquitin ligaseStress-induced accumulationRole of E6APUbiquitin ligaseProtein regulatorsTissue homeostasisReplicative senescenceCellular senescenceCell cycleStress responseImportant regulatorSenescenceStress conditionsE6APIndependent growthEnhanced growthEnhanced proliferationReplicativeRegulator