2017
The vascular endothelial specific IL-4 receptor alpha–ABL1 kinase signaling axis regulates the severity of IgE-mediated anaphylactic reactions
Yamani A, Wu D, Waggoner L, Noah T, Koleske AJ, Finkelman F, Hogan SP. The vascular endothelial specific IL-4 receptor alpha–ABL1 kinase signaling axis regulates the severity of IgE-mediated anaphylactic reactions. Journal Of Allergy And Clinical Immunology 2017, 142: 1159-1172.e5. PMID: 29157947, PMCID: PMC5957775, DOI: 10.1016/j.jaci.2017.08.046.Peer-Reviewed Original ResearchConceptsIgE-mediated anaphylactic reactionsAnaphylactic reactionsFluid extravasationIL-4RαBarrier dysfunctionIL-4Food-induced anaphylactic reactionsIgE-induced anaphylaxisFood-induced anaphylaxisIgE-mediated anaphylaxisIL-4 receptor α chainIgE-mediated reactionsTreatment of miceSevere anaphylactic reactionsSeverity of anaphylaxisABL kinase inhibitor imatinibKinase inhibitor imatinibReceptor α chainVe cell linesVenous vasodilatationOral antigenHypovolemic shockInhibitor imatinibAnaphylaxisVe cells
2016
The Src kinases Hck, Fgr and Lyn activate Arg to facilitate IgG-mediated phagocytosis and Leishmania infection
Wetzel DM, Rhodes EL, Li S, McMahon-Pratt D, Koleske AJ. The Src kinases Hck, Fgr and Lyn activate Arg to facilitate IgG-mediated phagocytosis and Leishmania infection. Journal Of Cell Science 2016, 129: 3130-3143. PMID: 27358479, PMCID: PMC5004897, DOI: 10.1242/jcs.185595.Peer-Reviewed Original ResearchMeSH KeywordsAniline CompoundsAnimalsCytokinesDisease Models, AnimalImatinib MesylateImmunoglobulin GLeishmaniaLeishmaniasisMacrophagesMiceModels, BiologicalNitrilesParasitesPhagocytosisPhosphorylationProtein-Tyrosine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-hckPyrimidinesQuinolinesRAW 264.7 CellsSignal TransductionSrc-Family KinasesConceptsAmastigote uptakeObligate intracellular parasite LeishmaniaImmunoglobulin-mediated phagocytosisIntracellular parasite LeishmaniaNovel therapeutic strategiesPersistence of infectionLeishmania infectionIgG-mediated phagocytosisTherapeutic strategiesFc receptorsSmall molecule inhibitorsArg activationDisease severityParasite burdenPrimary macrophagesMacrophagesKinase inhibitorsLeishmaniasisHuman hostDevastating diseaseInfectionParasite LeishmaniaSrc family kinasesPhagocytosisLeishmania
2012
The Abl and Arg Kinases Mediate Distinct Modes of Phagocytosis and Are Required for Maximal Leishmania Infection
Wetzel DM, McMahon-Pratt D, Koleske AJ. The Abl and Arg Kinases Mediate Distinct Modes of Phagocytosis and Are Required for Maximal Leishmania Infection. Molecular And Cellular Biology 2012, 32: 3176-3186. PMID: 22665498, PMCID: PMC3434515, DOI: 10.1128/mcb.00086-12.Peer-Reviewed Original ResearchConceptsComplement receptor 3Leishmania infectionIgG-coated beadsMurine cutaneous leishmaniasisPotential therapeutic targetLeishmania uptakeVisceral diseaseObligate intracellular parasitesCutaneous leishmaniasisTherapeutic targetFc receptorsAmastigote uptakeTreatment resultsReceptor 3Small lesionsInfection severityLeishmania amazonensisKinase inhibitorsIntracellular parasitesBead phagocytosisPhagocytosisReceptorsC3biInfectionLeishmaniasis
2007
Defective T Cell Development and Function in the Absence of Abelson Kinases
Gu JJ, Zhang N, He YW, Koleske AJ, Pendergast AM. Defective T Cell Development and Function in the Absence of Abelson Kinases. The Journal Of Immunology 2007, 179: 7334-7343. PMID: 18025176, DOI: 10.4049/jimmunol.179.11.7334.Peer-Reviewed Original ResearchConceptsT cell developmentT cellsMutant miceCell-autonomous roleT cell-dependent AgCD8 T cellsListeria monocytogenes infectionT cell expansionCell developmentNumber of thymocytesT cell functionDouble-positive stageDouble-negative populationDefective T cell developmentConditional knockout miceT cells resultsNull T cellsTCR-induced signalingCytokine productionMonocytogenes infectionAb productionKnockout miceThymocyte proliferationConditional deletionMiceDissecting kinase signaling pathways
Boyle SN, Koleske AJ. Dissecting kinase signaling pathways. Drug Discovery Today 2007, 12: 717-724. PMID: 17826684, DOI: 10.1016/j.drudis.2007.07.019.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntineoplastic AgentsBenzamidesDrug Delivery SystemsHumansImatinib MesylateLapatinibNeoplasmsPhosphoproteinsPhosphorylationPiperazinesProtein Kinase InhibitorsProtein KinasesProteomicsPyrimidinesQuinazolinesSignal TransductionTrastuzumabConceptsSame protein substrateProtein Kinase SignalingKinase substratePutative substratesProtein substratesKinase signalingProtein kinaseMultiple kinasesPhysiological substratesKinaseHuman diseasesDrug targetsPhysiological relevanceSubstrate interactionsKinase inhibitorsPathwaySignalingSubstrateNeurological disordersInteractionHallmarkInhibitorsTarget
2003
Abl Family Nonreceptor Tyrosine Kinases Modulate Short-Term Synaptic Plasticity
Moresco EM, Scheetz AJ, Bornmann WG, Koleske AJ, Fitzsimonds RM. Abl Family Nonreceptor Tyrosine Kinases Modulate Short-Term Synaptic Plasticity. Journal Of Neurophysiology 2003, 89: 1678-1687. PMID: 12626632, DOI: 10.1152/jn.00892.2002.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBenzamidesEnzyme InhibitorsHippocampusImatinib MesylateLong-Term PotentiationLong-Term Synaptic DepressionMiceMice, Mutant StrainsMicroscopy, ImmunoelectronNeuronal PlasticityOrgan Culture TechniquesPiperazinesProbabilityProtein-Tyrosine KinasesProto-Oncogene Proteins c-ablPyrimidinesSynapsesSynaptic TransmissionConceptsActin cytoskeletal dynamicsAbl family kinasesNonreceptor tyrosine kinasePaired-pulse facilitationCell morphogenesisMouse hippocampal area CA1Wild-type slicesActin cytoskeletonCytoskeletal dynamicsLong-term depressionLong-term potentiationFamily kinasesAdult mouse brainNonreceptor tyrosineTyrosine kinaseWild-type controlsFunctional interactionPostsynaptic compartmentsPosttetanic potentiationImmunoelectron microscopyMature neuronsImportant functionsKinaseBasal synaptic transmissionABL