2001
Requirement of the JIP1 scaffold protein for stress-induced JNK activation
Whitmarsh A, Kuan C, Kennedy N, Kelkar N, Haydar T, Mordes J, Appel M, Rossini A, Jones S, Flavell R, Rakic P, Davis R. Requirement of the JIP1 scaffold protein for stress-induced JNK activation. Genes & Development 2001, 15: 2421-2432. PMID: 11562351, PMCID: PMC312784, DOI: 10.1101/gad.922801.Peer-Reviewed Original ResearchConceptsJIP1 scaffold proteinSignal transduction pathwaysScaffold proteinTransduction pathwaysMAP kinase signal transduction pathwayJNK activationStress-induced JNK activationKinase signal transduction pathwayC-Jun N-terminal kinase (JNK) signal transduction pathwayExposure of cellsHomologous recombinationEnvironmental stressPrimary hippocampal neuronsC-JunAnoxic stressJIP1ProteinPathwayJNKExcitotoxic stressHippocampal neuronsActivationGenesStressCritical componentJNK3 contributes to c‐Jun activation and apoptosis but not oxidative stress in nerve growth factor‐deprived sympathetic neurons
Bruckner S, Tammariello S, Kuan C, Flavell R, Rakic P, Estus S. JNK3 contributes to c‐Jun activation and apoptosis but not oxidative stress in nerve growth factor‐deprived sympathetic neurons. Journal Of Neurochemistry 2001, 78: 298-303. PMID: 11461965, DOI: 10.1046/j.1471-4159.2001.00400.x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornApoptosisCells, CulturedGenes, junGenotypeIsoenzymesMiceMice, KnockoutMitogen-Activated Protein Kinase 10Mitogen-Activated Protein KinasesNerve Growth FactorNerve Tissue ProteinsNeuronsOxidative StressPhosphorylationProtein-Tyrosine KinasesProto-Oncogene Proteins c-junReverse Transcriptase Polymerase Chain ReactionSuperior Cervical GanglionConceptsJun kinaseC-Jun phosphorylationC-JunDominant negative proteinSympathetic neuronal deathProtein kinase pathwayOxidative stressC-jun inductionC-Jun activationPhosphorylated c-JunApoptotic roleJNK kinaseKinase pathwayNegative proteinJNK isoformsJNK pathwayOverall pathwayNeuronal deathSympathetic neuronsApoptosisJNK3NGF deprivationKinasePhosphorylationCritical role
1997
Absence of excitotoxicity-induced apoptosis in the hippocampus of mice lacking the Jnk3 gene
Yang D, Kuan C, Whitmarsh A, Rinócn M, Zheng T, Davis R, Rakic P, Flavell R. Absence of excitotoxicity-induced apoptosis in the hippocampus of mice lacking the Jnk3 gene. Nature 1997, 389: 865-870. PMID: 9349820, DOI: 10.1038/39899.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisDrug ResistanceExcitatory Amino Acid AgonistsGene ExpressionGene TargetingGlutamic AcidHippocampusKainic AcidMiceMice, Inbred C57BLMice, KnockoutMitogen-Activated Protein Kinase 10Mitogen-Activated Protein KinasesNeuronsPhosphorylationProtein KinasesProtein Serine-Threonine KinasesProtein-Tyrosine KinasesProto-Oncogene Proteins c-fosProto-Oncogene Proteins c-junSeizuresSignal TransductionTranscription Factor AP-1ConceptsKainic acidGlutamate receptor agonist kainic acidAgonist kainic acidExcitotoxicity-induced apoptosisExcitatory amino acidsHippocampal neuron apoptosisHippocampus of miceStress-induced neuronal apoptosisObserved neuroprotectionGlutamate neurotoxicitySeizure activityNeuron apoptosisGlutamate toxicityNeuronal apoptosisAP-1 transcription factor complexJNK3 geneMutant miceMiceMembrane depolarizationNoxious stressTranscription factor complexApoptosisC-JunRecent studiesTranscriptional activity