2017
Aging impairs both primary and secondary RIG-I signaling for interferon induction in human monocytes
Molony RD, Nguyen JT, Kong Y, Montgomery RR, Shaw AC, Iwasaki A. Aging impairs both primary and secondary RIG-I signaling for interferon induction in human monocytes. Science Signaling 2017, 10 PMID: 29233916, PMCID: PMC6429941, DOI: 10.1126/scisignal.aan2392.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAgingDEAD Box Protein 58FemaleHumansImmunity, InnateInterferonsMaleMonocytesReceptors, ImmunologicSignal TransductionConceptsType I IFNsI IFNsI interferonOlder adultsIFN inductionRetinoic acid-inducible gene IAcid-inducible gene IHealthy human donorsType I interferonRespiratory influenzaProinflammatory cytokinesVirus infectionType I IFN genesAdult monocytesAntiviral resistanceTranscription factor IRF8IFN responseHuman donorsMonocytesIncreased proteasomal degradationHuman monocytesYoung adultsIRF8 expressionIAV RNAInfected cellsMultiple network-constrained regressions expand insights into influenza vaccination responses
Avey S, Mohanty S, Wilson J, Zapata H, Joshi SR, Siconolfi B, Tsang S, Shaw AC, Kleinstein SH. Multiple network-constrained regressions expand insights into influenza vaccination responses. Bioinformatics 2017, 33: i208-i216. PMID: 28881994, PMCID: PMC5870750, DOI: 10.1093/bioinformatics/btx260.Peer-Reviewed Original Research
2015
Paradoxical changes in innate immunity in aging: recent progress and new directions
Montgomery RR, Shaw AC. Paradoxical changes in innate immunity in aging: recent progress and new directions. Journal Of Leukocyte Biology 2015, 98: 937-943. PMID: 26188078, PMCID: PMC4661037, DOI: 10.1189/jlb.5mr0315-104r.Peer-Reviewed Original ResearchMeSH KeywordsAgingAnimalsB-LymphocytesCytokinesHumansImmunity, InnateSignal TransductionT-LymphocytesConceptsImmune responseInnate immune changesInnate immune responseCytokine levelsInappropriate elevationImmune changesNaïve cell populationT cellsAdaptive immunityViral infectionParadoxical increaseInnate immunityMultiple cell typesParadoxical changesCell populationsActivation stateImmunityCell typesSevere consequencesResponseTissue contextImmunosenescenceVaccinationPopulationInfection
2014
Prolonged Proinflammatory Cytokine Production in Monocytes Modulated by Interleukin 10 After Influenza Vaccination in Older Adults
Mohanty S, Joshi SR, Ueda I, Wilson J, Blevins TP, Siconolfi B, Meng H, Devine L, Raddassi K, Tsang S, Belshe RB, Hafler DA, Kaech SM, Kleinstein SH, Trentalange M, Allore HG, Shaw AC. Prolonged Proinflammatory Cytokine Production in Monocytes Modulated by Interleukin 10 After Influenza Vaccination in Older Adults. The Journal Of Infectious Diseases 2014, 211: 1174-1184. PMID: 25367297, PMCID: PMC4366602, DOI: 10.1093/infdis/jiu573.Peer-Reviewed Original ResearchMeSH KeywordsAdultAge FactorsAgedCytokinesDual Specificity Phosphatase 1FemaleGene Expression RegulationGPI-Linked ProteinsHumansImmunity, InnateInfluenza VaccinesInfluenza, HumanInterleukin-10Interleukin-6Lipopolysaccharide ReceptorsMaleMonocytesPhosphorylationReceptors, IgGSignal TransductionSTAT3 Transcription FactorTumor Necrosis Factor-alphaVaccinationYoung AdultConceptsOlder adultsInfluenza vaccinationInflammatory monocytesInterleukin-10Cytokine productionOlder subjectsAnti-inflammatory cytokine interleukin-10Influenza vaccine antibody responseTumor necrosis factor αImpaired vaccine responsesVaccine antibody responseIL-10 productionCytokine interleukin-10Proinflammatory cytokine productionNecrosis factor αAge-associated elevationPhosphorylated signal transducerVaccine responsesAntibody responseInterleukin-6Immune responseMonocyte populationsDay 28Intracellular stainingVaccinationHuman monocytes have increased IFN-γ-mediated IL-15 production with age alongside altered IFN-γ receptor signaling
Lee N, Shin MS, Kang KS, Yoo SA, Mohanty S, Montgomery RR, Shaw AC, Kang I. Human monocytes have increased IFN-γ-mediated IL-15 production with age alongside altered IFN-γ receptor signaling. Clinical Immunology 2014, 152: 101-110. PMID: 24657713, PMCID: PMC4018768, DOI: 10.1016/j.clim.2014.03.003.Peer-Reviewed Original Research
2011
Age‐associated elevation in TLR5 leads to increased inflammatory responses in the elderly
Qian F, Wang X, Zhang L, Chen S, Piecychna M, Allore H, Bockenstedt L, Malawista S, Bucala R, Shaw AC, Fikrig E, Montgomery RR. Age‐associated elevation in TLR5 leads to increased inflammatory responses in the elderly. Aging Cell 2011, 11: 104-110. PMID: 22023165, PMCID: PMC3257374, DOI: 10.1111/j.1474-9726.2011.00759.x.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAgingExtracellular Signal-Regulated MAP KinasesFemaleHumansInflammationInterleukin-8MaleMiddle AgedMonocytesMultivariate AnalysisNF-kappa BP38 Mitogen-Activated Protein KinasesPhosphorylationProtein TransportRNA, MessengerSignal TransductionToll-Like Receptor 5Tumor Necrosis Factor-alphaConceptsToll-like receptorsIL-8Multivariable mixed-effects modelsOlder individualsElevated IL-8Levels of TLR5Expression of TLR5Production of TNFAge-associated elevationAge-related decreaseDendritic cellsImmune responsivenessElderly donorsInflammatory responseImmune functionNF-κBTLR5Progressive declineMonocytesMixed effects modelsMAPK p38Significant increaseEffects modelAssociated increaseCritical mechanism
2008
Defective signal transduction in B lymphocytes lacking presenilin proteins
Yagi T, Giallourakis C, Mohanty S, Scheidig C, Shen J, Zheng H, Xavier RJ, Shaw AC. Defective signal transduction in B lymphocytes lacking presenilin proteins. Proceedings Of The National Academy Of Sciences Of The United States Of America 2008, 105: 979-984. PMID: 18195359, PMCID: PMC2242696, DOI: 10.1073/pnas.0707755105.Peer-Reviewed Original ResearchConceptsPresenilin proteinsDiverse cellular processesMultiple genomic datasetsPS proteinsSignal transduction eventsWhole-genome datasetsDefective signal transductionNotch family membersCalcium-dependent signalingCellular processesProtein substratesSignal transductionTransduction eventsProtein interactionsPS2 functionUnanticipated roleConditional alleleGenomic datasetsToll-like receptor signalingPathway analysisIntegrative analysisPosttranslational cleavageReceptor signalingRecombinase expressionProtein
1999
Induction of Ig light chain gene rearrangement in heavy chain-deficient B cells by activated Ras
Shaw A, Swat W, Davidson L, Alt F. Induction of Ig light chain gene rearrangement in heavy chain-deficient B cells by activated Ras. Proceedings Of The National Academy Of Sciences Of The United States Of America 1999, 96: 2239-2243. PMID: 10051625, PMCID: PMC26767, DOI: 10.1073/pnas.96.5.2239.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBase SequenceBlastocystB-LymphocytesCell DifferentiationDNA-Binding ProteinsEmbryo, MammalianGene Rearrangement, B-Lymphocyte, Light ChainGenes, ImmunoglobulinImmunoglobulin Heavy ChainsImmunoglobulin kappa-ChainsImmunoglobulin Light ChainsImmunoglobulin Variable RegionKidneyMiceMolecular Sequence DataRas ProteinsRecombinant Fusion ProteinsSignal TransductionSpleenStem CellsTransfectionConceptsRas expressionVariable region gene assemblyEmbryonic stem cellsIg light chain gene rearrangementGene rearrangementsB cell developmentWild-type B cellsB lineage cellsLight chain gene rearrangementsDevelopmental checkpointsHeavy chain geneGene productsGene assemblyExpression constructsB cell differentiationGene expressionBlastocyst complementationIg heavy chain genesCell developmentCell differentiationVariable region genesB cellsDifferentiation potentialLineage cellsChain gene
1991
Cytoplasmic tail deletion converts membrane immunoglobulin to a phosphatidylinositol-linked form lacking signaling and efficient antigen internalization functions
Mitchell RN, Shaw AC, Weaver YK, Leder P, Abbas AK. Cytoplasmic tail deletion converts membrane immunoglobulin to a phosphatidylinositol-linked form lacking signaling and efficient antigen internalization functions. Journal Of Biological Chemistry 1991, 266: 8856-8860. PMID: 2026599, DOI: 10.1016/s0021-9258(18)31524-2.Peer-Reviewed Original ResearchConceptsPhosphatidylinositol-linked formSignal transduction functionsPhosphatidylinositol-linked proteinsB cell lymphoma A20Cytoplasmic domainCytoplasmic tailMembrane proteinsSignal transductionTransmembrane proteinTransmembrane residuesTransduction functionMolecular massInternalization functionProteinAntigen receptorAntigen presentationEarly eventsMembrane immunoglobulinIg moleculesMode of expressionTransductionMIgMB lymphocytesSignalingResidues
1990
Mutations of immunoglobulin transmembrane and cytoplasmic domains: Effects on intracellular signaling and antigen presentation
Shaw A, Mitchell R, Weaver Y, Campos-Torres J, Abbas A, Leder P. Mutations of immunoglobulin transmembrane and cytoplasmic domains: Effects on intracellular signaling and antigen presentation. Cell 1990, 63: 381-392. PMID: 2119890, DOI: 10.1016/0092-8674(90)90171-a.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsAntibody FormationAntigensBase SequenceB-LymphocytesCalciumCell LineCell MembraneCytoplasmHumansImmunoglobulin mu-ChainsKineticsMiceMolecular Sequence DataMutagenesis, Site-DirectedOligonucleotide ProbesReceptors, Antigen, B-CellSequence Homology, Nucleic AcidSignal TransductionTransfectionConceptsCytoplasmic domainSignal transductionShort cytoplasmic domainDifferent protein interactionsMembrane-bound formMu chain geneProtein interactionsTransmembrane residuesIntracellular signalingChain geneSpecific mutationsTransductionAntigen presentationAntigen-specific receptorsMutationsTransmembraneB cellsGenesSignalingDomainResiduesCellsAssaysReceptors