grant

Induction of myeloid-epithelial gap junctional channels to enhance host resilience against acute lung injury.

Organization COLUMBIA UNIVERSITY HEALTH SCIENCESLocation NEW YORK, UNITED STATESPosted 17 Jun 2024Deadline 31 May 2028
NIHUS FederalResearch GrantFY2025(hydroxymethylglutaryl-CoA reductase (NADPH)) kinase5'-AMP-activated protein kinaseAMP KinaseAMP-activated kinaseAMP-activated protein kinaseAMPK enzymeARDSATP-AMP PhosphotransferaseATP-AMP TransphosphorylaseActive Follow-upAcute Lung InjuryAcute Pulmonary InjuryAcute Respiratory DistressAcute Respiratory Distress SyndromeAddressAdenylokinaseAdult ARDSAdult RDSAdult Respiratory Distress SyndromeAlveolarAlveolar MacrophagesAlveolusAnti-InflammatoriesAnti-Inflammatory AgentsAnti-inflammatoryAssayBacteriaBioassayBiological AssayBloodBlood Reticuloendothelial SystemBlood monocyteBone MarrowBone Marrow Reticuloendothelial SystemBronchial AlveolusCa(2+)-Calmodulin Dependent Protein KinaseCaMKCalciumCalcium/calmodulin-dependent protein kinaseCalmodulin-Binding ProteinsCalmodulin-Dependent Protein KinasesCalmodulin-KinaseCell BodyCell Communication and SignalingCell SignalingCell TherapyCellsCommunicating JunctionCommunicationConfocal MicroscopyConnexin 43Connexin43Cx43Da Nang LungDataEpitheliumFrequenciesGap JunctionsGene ModifiedGram-Negative BacteriaHMG CoA reductase (NADPH) kinaseHMG CoA reductase kinaseHMG coenzyme A reductase (NADPH) kinaseHeterogeneityHumanImmunoglobulin Enhancer-Binding ProteinInflammatoryIntracellular Communication and SignalingKinasesKnock-outKnockoutLavageLipopolysaccharidesLow-resistance JunctionLungLung Alveolar EpitheliaLung InflammationLung ParenchymaLung Respiratory SystemLung TissueMarrow monocyteMiceMice MammalsModern ManMurineMusMyelogenousMyeloidMyeloid CellsMyokinaseNF-kBNF-kappa BNF-kappaBNFKBNexus JunctionNuclear Factor kappa BNuclear Transcription Factor NF-kBOutcomeP aeruginosaP. aeruginosaPatternPhosphorylationPhosphotransferase GenePhosphotransferasesPneumonitisProtein PhosphorylationPseudomonas aeruginosaPseudomonas pyocyaneaPulmonary InflammationPulmonary MacrophagesPulmonary imagingReportingResearchRoleShock LungSignal TransductionSignal Transduction SystemsSignalingSliceStiff lungStructure of parenchyma of lungTestingTimeTranscription Factor NF-kBTransmissionTransphosphorylasesactive followupadenylate kinasealveolar epitheliumbiological signal transductionbuild resiliencebuild resiliencycalcium-calmodulin-dependent PKcalcium-calmodulin-dependent PK type IIcalmodulin dependent protein kinasecell based interventioncell mediated interventioncell mediated therapiescell-based therapeuticcell-based therapycellular therapeuticcellular therapydevelop resiliencedevelop resiliencyenhance resilienceenhance resiliencyexperimentexperimental researchexperimental studyexperimentsfacilitate resiliencefollow upfollow-upfollowed upfollowupgap junction channelgene modificationgenetically modifiedhydroxymethylglutaryl-CoA-reductase kinaseimprove resilienceimprove resiliencyincrease resilienceincrease resiliencyinterestkappa B Enhancer Binding Proteinknock-downknockdownlavage therapylung imaginglung scanningmicrotubule associated protein 2 kinasemonocytemortalitymouse modelmurine modelnovelnuclear factor kappa betaopportunistic pathogenpromote resiliencepromote resiliencyprotective effectprotein kinase IIreal-time imagesrealtime imageresilienceresilience developmentresilience factorresiliency factorresilientresponsesexsocial roletransmission processwet lung
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PROJECT SUMMARY
Significance. Better understanding is required of innate mechanisms and new cell therapies that enhance

host resilience against acute lung injury (ALI), and the associated acute respiratory distress syndrome (ARDS).

Based on our prior findings, our premise is that gap junctional channels (GJCs) between myeloid cells and the…

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Induction of myeloid-epithelial gap junctional channels to enhance host resilience against acute lung injury. — COLUMBIA | Dev Procure