2014
An ENU-induced splicing mutation reveals a role for Unc93b1 in early immune cell activation following influenza A H1N1 infection
Lafferty EI, Flaczyk A, Angers I, Homer R, d'Hennezel E, Malo D, Piccirillo CA, Vidal SM, Qureshi ST. An ENU-induced splicing mutation reveals a role for Unc93b1 in early immune cell activation following influenza A H1N1 infection. Genes & Immunity 2014, 15: 320-332. PMID: 24848930, PMCID: PMC4978536, DOI: 10.1038/gene.2014.22.Peer-Reviewed Original ResearchMeSH KeywordsAlternative SplicingAnimalsCD8-Positive T-LymphocytesChemokine CXCL10EndosomesEthylnitrosoureaImmunity, InnateInfluenza A Virus, H1N1 SubtypeInterferon Type IInterferon-gammaL-SelectinLungLymphocyte ActivationMacrophage ActivationMembrane Transport ProteinsMiceMice, Inbred C57BLMutationOrthomyxoviridae InfectionsToll-Like ReceptorsConceptsEndosomal TLRsImmune responseEndosomal Toll-like receptorsInfluenza A/PR/8/34Expression of CXCL10Toll-like receptorsImmune cell activationCD69 activation markerInnate immune responseHuman infectious diseasesViral clearanceActivation markersInfected lungsRespiratory pathogensTLR responsesT cellsLymphoid cellsCell activationTissue pathologyInfectious diseasesMouse strainsInfectionExudate macrophagesReduced expressionUNC93B1
2006
Essential role of nitric oxide in VEGF-induced, asthma-like angiogenic, inflammatory, mucus, and physiologic responses in the lung
Bhandari V, Choo-Wing R, Chapoval SP, Lee CG, Tang C, Kim YK, Ma B, Baluk P, Lin MI, McDonald DM, Homer RJ, Sessa WC, Elias JA. Essential role of nitric oxide in VEGF-induced, asthma-like angiogenic, inflammatory, mucus, and physiologic responses in the lung. Proceedings Of The National Academy Of Sciences Of The United States Of America 2006, 103: 11021-11026. PMID: 16832062, PMCID: PMC1544167, DOI: 10.1073/pnas.0601057103.Peer-Reviewed Original ResearchConceptsInducible NOSNitric oxideEndothelial NOS inhibitorDendritic cell activationNO-dependent mechanismAirway hyperresponsivenessMucus metaplasiaLymphocyte accumulationPulmonary alterationsCell hyperplasiaNOS inhibitorNormal micePhysiologic responsesCell activationInflammationENOSVEGFMiceIndependent mechanismsTissue responseLatter responseLungAngiogenesisRemodelingNull mutation