Defects in actin-cap formation in Vav-deficient mice implicate an actin requirement for lymphocyte signal transduction
Holsinger L, Graef I, Swat W, Chi T, Bautista D, Davidson L, Lewis R, Alt F, Crabtree G. Defects in actin-cap formation in Vav-deficient mice implicate an actin requirement for lymphocyte signal transduction. Current Biology 1998, 8: 563-573. PMID: 9601640, DOI: 10.1016/s0960-9822(98)70225-8.Peer-Reviewed Original ResearchMeSH KeywordsActinsAnimalsCell Cycle ProteinsCytoskeletonDNA-Binding ProteinsHumansJurkat CellsMiceNFATC Transcription FactorsNuclear ProteinsProto-Oncogene ProteinsProto-Oncogene Proteins c-vavReceptor-CD3 Complex, Antigen, T-CellReceptors, Antigen, T-CellSignal TransductionT-LymphocytesTranscription FactorsTranscription, GeneticConceptsMitogen-activated protein kinaseCap formationActin polymerizationGuanine nucleotide exchange factorsJun N-terminal kinaseTranscription factor NF-ATc1Vav-deficient miceActin-dependent pathwayStress-activated kinasesGrowth regulatory signalsActin cap formationAntigen receptor signalingEgr-1 geneLymphocyte signal transductionN-terminal kinaseAntigen-receptor interactionActin cytoskeletonExchange factorTranscriptional inductionSignal transductionDependent transcriptionProtein kinaseGTPase RacRegulatory signalsNull mutation