2014
Rif1 Maintains Telomere Length Homeostasis of ESCs by Mediating Heterochromatin Silencing
Dan J, Liu Y, Liu N, Chiourea M, Okuka M, Wu T, Ye X, Mou C, Wang L, Wang L, Yin Y, Yuan J, Zuo B, Wang F, Li Z, Pan X, Yin Z, Chen L, Keefe DL, Gagos S, Xiao A, Liu L. Rif1 Maintains Telomere Length Homeostasis of ESCs by Mediating Heterochromatin Silencing. Developmental Cell 2014, 29: 7-19. PMID: 24735877, PMCID: PMC4720134, DOI: 10.1016/j.devcel.2014.03.004.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsEmbryonic Stem CellsGene DeletionGene Expression Regulation, DevelopmentalGene SilencingHeterochromatinHistonesMethylationMiceProtein BindingProtein Processing, Post-TranslationalRecombination, GeneticRNA, MessengerTelomereTelomere HomeostasisTelomere-Binding ProteinsTranscription FactorsConceptsTelomere length homeostasisEmbryonic stem cellsLength homeostasisZscan4 expressionHeterochromatic silencingHeterochromatin silencingMethylation complexChromosomal fusionsEmbryonic lethalityGenomic stabilityTelomere elongationH3K9me3 levelsSubtelomeric regionsRecombination defectsLength heterogeneityStem cellsRIF1HomeostasisSilencingExpressionZscan4HyperrecombinationShRNALethalityInteracts
2013
Depleting the methyltransferase Suv39h1 improves DNA repair and extends lifespan in a progeria mouse model
Liu B, Wang Z, Zhang L, Ghosh S, Zheng H, Zhou Z. Depleting the methyltransferase Suv39h1 improves DNA repair and extends lifespan in a progeria mouse model. Nature Communications 2013, 4: 1868. PMID: 23695662, PMCID: PMC3674265, DOI: 10.1038/ncomms2885.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsDisease Models, AnimalDNA DamageDNA RepairEnzyme StabilityFibroblastsHEK293 CellsHeterochromatinHistonesHumansLamin Type ALongevityLysineMethylationMethyltransferasesMiceNuclear ProteinsProgeriaProtein BindingProtein PrecursorsProtein Processing, Post-TranslationalRepressor ProteinsConceptsHutchinson-Gilford progeria syndromeBody weight lossBone mineral densityProgeria syndromeDNA repair capacityMineral densityMouse modelProgeria mouse modelG608G mutationSyndromeWeight lossProgeroid featuresRepair capacityH3K9me3 levelsPremature agingG mutationPotential strategyEpigenetic alterations
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply