2020
m6A Modification Prevents Formation of Endogenous Double-Stranded RNAs and Deleterious Innate Immune Responses during Hematopoietic Development
Gao Y, Vasic R, Song Y, Teng R, Liu C, Gbyli R, Biancon G, Nelakanti R, Lobben K, Kudo E, Liu W, Ardasheva A, Fu X, Wang X, Joshi P, Lee V, Dura B, Viero G, Iwasaki A, Fan R, Xiao A, Flavell RA, Li HB, Tebaldi T, Halene S. m6A Modification Prevents Formation of Endogenous Double-Stranded RNAs and Deleterious Innate Immune Responses during Hematopoietic Development. Immunity 2020, 52: 1007-1021.e8. PMID: 32497523, PMCID: PMC7408742, DOI: 10.1016/j.immuni.2020.05.003.Peer-Reviewed Original ResearchConceptsDouble-stranded RNADeleterious innate immune responseMammalian hematopoietic developmentEndogenous double-stranded RNAHematopoietic developmentInnate immune responseAbundant RNA modificationMurine fetal liverPattern recognition receptor pathwaysImmune responseProtein codingDsRNA formationRNA modificationsWriter METTL3Hematopoietic defectsPerinatal lethalityNative stateConditional deletionAberrant innate immune responsesLoss of METTL3Hematopoietic failureReceptor pathwayAberrant immune responsePrevents formationFetal liver
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
2008
Methylation of RUNX1 by PRMT1 abrogates SIN3A binding and potentiates its transcriptional activity
Zhao X, Jankovic V, Gural A, Huang G, Pardanani A, Menendez S, Zhang J, Dunne R, Xiao A, Erdjument-Bromage H, Allis CD, Tempst P, Nimer SD. Methylation of RUNX1 by PRMT1 abrogates SIN3A binding and potentiates its transcriptional activity. Genes & Development 2008, 22: 640-653. PMID: 18316480, PMCID: PMC2259033, DOI: 10.1101/gad.1632608.Peer-Reviewed Original ResearchMeSH KeywordsAntigens, CD34ArginineCell Line, TumorCore Binding Factor Alpha 2 SubunitDNA-Binding ProteinsGene Expression RegulationHematopoiesisHumansMethylationMutationPlatelet Membrane Glycoprotein IIbProtein-Arginine N-MethyltransferasesProto-Oncogene ProteinsRepressor ProteinsRNA, Small InterferingRUNX1 Translocation Partner 1 ProteinSin3 Histone Deacetylase and Corepressor ComplexTrans-ActivatorsTranscription FactorsTranscription, GeneticConceptsRUNX1 functionArginine residuesRUNX1-ETO fusion proteinArginine methyltransferase PRMT1Arginine methylation sitesPRMT1-dependent methylationRUNX1 target genesProtein-protein interactionsPost-translational modificationsRUNX1/AML1Dominant inhibitory activityDefinitive hematopoiesisMethyltransferase PRMT1Corepressor Sin3ATranscriptional coactivatorPRMT1Target genesMethylation sitesDynamic regulationTranscriptional activityCorepressor bindingHuman acute leukemiaFusion proteinChromosome translocationRUNX1