grant
Chromatin Regulation of Immune Cells in Myocardial Inflammation
Organization J. DAVID GLADSTONE INSTITUTESLocation SAN FRANCISCO, UNITED STATESPosted 12 Sept 2025Deadline 31 May 2030
NIHUS FederalResearch GrantFY2025AcuteAcute myocardial infarctAcute myocardial infarctionAddressAdoptedAffectAllelesAllelomorphsAutomobile DrivingB220BET bromodomain inhibitorBET inhibitorBETiBRD2BRD2 geneBasal Transcription FactorBasal transcription factor genesBindingBinding SitesBlood monocyteBone MarrowBone Marrow Reticuloendothelial SystemBromodomainBromodomain and Extra-Terminal motif inhibitorBromodomains and extra-terminal domain inhibitorCCL2CCL2 geneCD45CRISPR interferenceCRISPR-dCas9-mediated repressionCRISPR/dCas9 interferenceCRISPR/dCas9-mediated transcriptional inhibitionCRISPRiCUT&RUNCardiacCardiac Failure CongestiveCardiac Muscle CellsCardiac MyocytesCardiac infarctionCardiocyteCell BodyCell Communication and SignalingCell SignalingCellsChemokine, CC Motif, Ligand 2ChromatinChronicCicatrixCleavage Targets and Release Using NucleaseCleavage Under Targets and Release Using NucleaseClustered Regularly Interspaced Short Palindromic Repeats interferenceCombining SiteCongestive Heart FailureD6S113EDataDevelopmentDistalDysfunctionElementsEnhancersEpigeneticEpigenetic ChangeEpigenetic MechanismEpigenetic ProcessFSRG1Female Sterile Homeotic-Related Gene 1FibrosisFibrosis in the heartFibrosis in the myocardiumFibrosis within the heartFibrosis within the myocardiumFibrotic myocardiumFlow CytofluorometriesFlow CytofluorometryFlow CytometryFlow MicrofluorimetryFlow MicrofluorometryFunctional disorderFutureGP180Gene ExpressionGene TranscriptionGeneral Transcription Factor GeneGeneral Transcription FactorsGenesGeneticGenetic TranscriptionGoalsHeartHeart DecompensationHeart Muscle CellsHeart failureHeart myocyteImmuneImmune TargetingImmune infiltratesImmune responseImmunesImmunomodulationImpairmentInfiltrationInflammationInflammatoryInflammatory ResponseInjuryInnate Immune SystemIntracellular Communication and SignalingIschemic HeartIschemic Heart DiseaseIschemic myocardiumKI miceKIAA9001Knock-in MouseLY5LigandsLoxP-flanked alleleMCAFMCP-1MCP1MacrophageMacrophage ActivationMapsMarrow monocyteMass Photometry/Spectrum AnalysisMass SpectrometryMass SpectroscopyMass SpectrumMass Spectrum AnalysesMass Spectrum AnalysisMediatingMiceMice MammalsMolecular InteractionMonocyte Chemoattractant Protein-1Monocyte Chemotactic Protein-1Monocyte Chemotactic and Activating FactorMonocyte Chemotactic and Activating ProteinMonocyte Chemotactive and Activating FactorMonocyte Secretory Protein JEMorbidityMorbidity - disease rateMurineMusMyocardialMyocardial InfarctMyocardial InfarctionMyocardial IschemiaMyocarditisMφPTPRCPTPRC genePathologicPathway interactionsPatientsPhasePhenotypePhysiologicPhysiologicalPhysiopathologyPlayProcessProtein FamilyProteinsProteomicsPublic HealthRING3RNA ExpressionRNF3Reactive SiteReceptor ProteinRegulatory ElementRepressionResearchRiskRoleRuptureSCYA2ScarsShapesSignal TransductionSignal Transduction SystemsSignalingSingle-Nucleus SequencingSmall Inducible Cytokine A2SortingSpecific qualifier valueSpecifiedStressT200TestingTherapeuticTimeTracerTranscriptionTranscription Factor Proto-OncogeneTranscription factor genesVentricularWorkWound Repairbiological signal transductionbromodomain extra-terminal inhibitorcardiac failurecardiac fibrosiscardiac functioncardiac infarctcardiac inflammationcardiac ischemiacardiomyocytechronic heart failurecoronary attackcoronary fibrosiscoronary infarctcoronary infarctioncoronary ischemiadevelop therapydevelopmentaldrivingepigeneticallyepigenomicsexperimentexperimental researchexperimental studyexperimentsfibrotic heartflow cytophotometryfloxedfloxed allelefunction of the heartgene regulatory networkgenome scalegenome-widegenomewidehealingheart attackheart fibrosisheart functionheart infarctheart infarctionheart ischemiahost responseimmune cell infiltrateimmune modulationimmune regulationimmune system responseimmunologic reactivity controlimmunomodulatoryimmunoregulationimmunoregulatoryimmunoresponseimprovedimproved outcomeinjuriesintervention developmentknockin micemembermonocytemortalitymouse modelmulti-modalitymultimodalitymurine modelmyocardial fibrosismyocardial ischemia/hypoxiamyocardium ischemianew drug targetnew druggable targetnew pharmacotherapy targetnew therapeutic targetnew therapy targetnovelnovel drug targetnovel druggable targetnovel pharmacotherapy targetnovel therapeutic targetnovel therapy targetpathophysiologypathwaypharmacologicpreservationpressurepreventpreventingprogramsreceptorrecruitrepair functionreparative functionrepressing CRISPR-dCas9 systemsNuc-SeqscATAC sequencingscATAC-seqscRNA sequencingscRNA-seqsingle cell ATAC-seqsingle cell ATAC-sequencingsingle cell Assay for Transposase Accessible Chromatin sequencingsingle cell RNA-seqsingle cell RNAseqsingle cell expression profilingsingle cell sequencing assay for transposase accessible chromatinsingle cell transcriptomic profilingsingle nucleus RNA-sequencingsingle nucleus seqsingle-cell Assay for Transposase-Accessible Chromatin with sequencingsingle-cell RNA sequencingsingle-cell assay for transposase-accessible chromatin using sequencingsingle-cell assay for transposase-accessible chromatin-seqsingle-nucleus RNA-seqsnRNA sequencingsnRNA-seqsocial rolesystemic toxicitytherapy developmenttissue repairtranscription factortreatment developmentwound healingwound recoverywound resolution
Description preview
PROJECT SUMMARY
Ischemic heart disease following myocardial infarction (MI) is a leading cause of global morbidity and mortality.
During MI, infiltrating immune cells, particularly monocytes, differentiate into macrophages, adopting both
reparative and maladaptive pro-inflammatory roles. These maladaptive immune responses can drive chronic…
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