2012
E6AP ubiquitin ligase regulates PML-induced senescence in Myc-driven lymphomagenesis
Wolyniec K, Shortt J, de Stanchina E, Levav-Cohen Y, Alsheich-Bartok O, Louria-Hayon I, Corneille V, Kumar B, Woods S, Opat S, Johnstone R, Scott C, Segal D, Pandolfi P, Fox S, Strasser A, Jiang Y, Lowe S, Haupt S, Haupt Y. E6AP ubiquitin ligase regulates PML-induced senescence in Myc-driven lymphomagenesis. Blood 2012, 120: 822-832. PMID: 22689861, PMCID: PMC3709628, DOI: 10.1182/blood-2011-10-387647.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBurkitt LymphomaCell Line, TumorCell Transformation, NeoplasticCellular SenescenceHumansLymphoma, Large B-Cell, DiffuseMiceMice, Inbred C57BLMice, TransgenicNuclear ProteinsPromyelocytic Leukemia ProteinProteasome Endopeptidase ComplexProto-Oncogene Proteins c-mycTranscription FactorsTumor Suppressor ProteinsUbiquitinUbiquitin-Protein LigasesConceptsB-cell lymphomaB-cell lymphomagenesisCellular senescenceB-cell lymphoma developmentNon-Hodgkin lymphomaNovel therapeutic approachesB-cell lymphoma progressionHuman Burkitt lymphomaTumor-suppressive actionB lymphoma cellsTherapeutic approachesBurkitt's lymphomaLymphoma progressionSuppressive actionLymphoma developmentLymphomaConcurrent inductionE6AP ubiquitin ligasePML expressionElevated levelsE6AP expressionKey tumor suppressorPML nuclear bodiesNeoplastic transformationLymphomagenesis
2009
E6AP promotes the degradation of the PML tumor suppressor
Louria-Hayon I, Alsheich-Bartok O, Levav-Cohen Y, Silberman I, Berger M, Grossman T, Matentzoglu K, Jiang Y, Muller S, Scheffner M, Haupt S, Haupt Y. E6AP promotes the degradation of the PML tumor suppressor. Cell Death & Differentiation 2009, 16: 1156-1166. PMID: 19325566, DOI: 10.1038/cdd.2009.31.Peer-Reviewed Original ResearchConceptsPML-NBsNuclear bodiesTumor suppressorPromyelocytic leukemia (PML) tumor suppressorE3 ligase E6APPML tumor suppressorPML nuclear bodiesPML protein expressionUbiquitination assaysCertain human cancersStress signalsPML proteinImportant regulatorPML stabilityDNA damageE6APCell typesHuman cancersProtein expressionActive formNull micePhysiological levelsSuppressorGrowth inhibitionPML
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