2020
The role of Hipk2-p53 pathways in arsenic-induced autistic behaviors: A translational study from rats to humans
Zhou H, Lin Y, Zhao W, Teng Y, Cui Y, Wang T, Li C, Jiang YH, Zhang JJ, Wang Y. The role of Hipk2-p53 pathways in arsenic-induced autistic behaviors: A translational study from rats to humans. Environmental Pollution 2020, 267: 115568. PMID: 33254717, DOI: 10.1016/j.envpol.2020.115568.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsArsenicAutism Spectrum DisorderAutistic DisorderCarrier ProteinsCase-Control StudiesChildHumansProtein Serine-Threonine KinasesRatsTumor Suppressor Protein p53ConceptsCase-control studySerum levelsArsenic exposureHealthy controlsNeuronal apoptosisFrontal cortexAge-matched healthy controlsGestational arsenic exposureHuman case-control studiesASD developmentHigher serum levelsAutistic behaviorASD childrenDose-dependent mannerAutism spectrum disorderPotential mediating pathwaysRat modelRat pupsKey molecular changesImmunohistochemistry analysisTranslational studiesWestern blottingMolecular changesTranslational strategiesMediating pathways
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
2003
Requirement of e6ap and the features of human papillomavirus e6 necessary to support degradation of p53
Cooper B, Schneider S, Bohl J, Jiang Y, Beaudet A, Pol S. Requirement of e6ap and the features of human papillomavirus e6 necessary to support degradation of p53. Virology 2003, 306: 87-99. PMID: 12620801, DOI: 10.1016/s0042-6822(02)00012-0.Peer-Reviewed Original Research
1998
Mutation of the Angelman Ubiquitin Ligase in Mice Causes Increased Cytoplasmic p53 and Deficits of Contextual Learning and Long-Term Potentiation
Jiang Y, Armstrong D, Albrecht U, Atkins C, Noebels J, Eichele G, Sweatt J, Beaudet A. Mutation of the Angelman Ubiquitin Ligase in Mice Causes Increased Cytoplasmic p53 and Deficits of Contextual Learning and Long-Term Potentiation. Neuron 1998, 21: 799-811. PMID: 9808466, DOI: 10.1016/s0896-6273(00)80596-6.Peer-Reviewed Original ResearchConceptsLong-term potentiationMaternal deficiencyAngelman syndromeNormal baseline synaptic transmissionBaseline synaptic transmissionE6-AP ubiquitinMotor dysfunctionSynaptic transmissionPhenotype of miceMice causesPotential biochemical basisPostmitotic neuronsLearning deficitsMiceDegradation of p53E6 proteinPotentiationP53Cytoplasmic p53UBE3ACytoplasmic abundanceDeficitsDeficiencyPhenotypeBiochemical basis