2016
Isoform Switch of TET1 Regulates DNA Demethylation and Mouse Development
Zhang W, Xia W, Wang Q, Towers AJ, Chen J, Gao R, Zhang Y, Yen CA, Lee AY, Li Y, Zhou C, Liu K, Zhang J, Gu TP, Chen X, Chang Z, Leung D, Gao S, Jiang YH, Xie W. Isoform Switch of TET1 Regulates DNA Demethylation and Mouse Development. Molecular Cell 2016, 64: 1062-1073. PMID: 27916660, DOI: 10.1016/j.molcel.2016.10.030.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBinding SitesChromatinCpG IslandsDNA-Binding ProteinsEmbryo, MammalianGene Expression Regulation, DevelopmentalGenomic ImprintingMaleMiceMouse Embryonic Stem CellsOvumPromoter Regions, GeneticProtein BindingProtein Interaction Domains and MotifsProtein IsoformsProto-Oncogene ProteinsSpermatozoaConceptsPrimordial germ cellsEmbryonic stem cellsCpG islandsChromatin bindingDNA demethylationMouse developmentDNA-binding modulesCXXC domainTET proteinsEarly embryosSomatic cellsN-terminusDevelopmental defectsShort isoformExclusive expressionTET1Germ cellsIsoform switchStem cellsDemethylationIsoformsCellsBindingImportant roleTerminus
2003
Disruption of the genomic imprint in trans with homologous recombination at Snrpn in ES cells
Tsai T, Bressler J, Jiang Y, Beaudet AL. Disruption of the genomic imprint in trans with homologous recombination at Snrpn in ES cells. Genesis 2003, 37: 151-161. PMID: 14666508, DOI: 10.1002/gene.10237.Peer-Reviewed Original ResearchConceptsPaternal alleleImprinting centerMaternal alleleSomatic mammalian cellsTrans-acting factorsActivation of expressionSNURF-SNRPN geneMouse ES cellsChromatin domainsGenomic imprintsImprinted domainMammalian cellsHomologous recombinationGene targetingHomologous associationES cellsComplete demethylationSNURF-SNRPNPrader-Willi syndromeExon 2AllelesGenesRecombinantsCellsDomain
1999
Mutation of the E6-AP Ubiquitin Ligase Reduces Nuclear Inclusion Frequency While Accelerating Polyglutamine-Induced Pathology in SCA1 Mice
Cummings C, Reinstein E, Sun Y, Antalffy B, Jiang Y, Ciechanover A, Orr H, Beaudet A, Zoghbi H. Mutation of the E6-AP Ubiquitin Ligase Reduces Nuclear Inclusion Frequency While Accelerating Polyglutamine-Induced Pathology in SCA1 Mice. Neuron 1999, 24: 879-892. PMID: 10624951, DOI: 10.1016/s0896-6273(00)81035-1.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAtaxin-1AtaxinsCell NucleusCells, CulturedCysteine EndopeptidasesFluorescent Antibody TechniqueHeLa CellsHumansImmunoblottingImmunohistochemistryInclusion BodiesLigasesMiceMice, KnockoutMicroscopy, ConfocalMultienzyme ComplexesMutationNerve Tissue ProteinsNuclear ProteinsPeptidesPhenotypePlasmidsProteasome Endopeptidase ComplexPurkinje CellsSpinocerebellar DegenerationsUbiquitin-Protein LigasesUbiquitinsConceptsMutant ataxin-1Ataxin-1Spinocerebellar ataxia type 1Ataxin-1 aggregationUbiquitin-protein ligaseUbiquitin-positive nuclear inclusionsUbiquitin-proteasome pathwayNuclear inclusionsPolyglutamine proteinsProteasomal degradationProteasome distributionMutant formsSCA1 pathogenesisAtaxia type 1Patient neuronsPurkinje cell pathologySCA1 miceCell pathologyInclusion frequencyCellsLigasePurkinje cellsProtein