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Defining the Pathogenic Contribution of High Genotypic MIF Expression
Organization YALE UNIVERSITYLocation NEW HAVEN, UNITED STATESPosted 1 Jun 2021Deadline 30 Apr 2026 β οΈ
NIHUS FederalResearch GrantFY2025AccelerationAdoptive TransferAllelesAllelomorphsAngiitisArthritisAtrophic ArthritisAutoimmune DiseasesBasal Transcription FactorBasal transcription factor genesBindingBiological Response Modifier TherapyBiological TherapyBloodBlood Reticuloendothelial SystemBody TissuesCD44CD44 geneCardiovascular DiseasesCell BodyCell Communication and SignalingCell Culture TechniquesCell SignalingCellsChronic Childhood ArthritisClinicalClinical EvaluationClinical TestingCollagenDataDiarthrosisDiseaseDisease ProgressionDisorderEvaluationExonsExperimental ArthritisFc ReceptorFibroblastsGeneral Transcription Factor GeneGeneral Transcription FactorsGenesGeneticGenetic PolymorphismGenotypeGlucocorticoidsHumanHuman Migration / DistributionImmunologyInduction of ApoptosisInflammationInflammatoryInflammatory ArthritisIntracellular Communication and SignalingIsoformsJoint DiseasesJointsJuvenile Chronic ArthritisJuvenile Chronic PolyarthritisJuvenile Rheumatoid ArthritisLaboratoriesLupus Erythematosus DisseminatusMDU3MacrophageMacrophage Migration Inhibition FactorsMacrophage Migration Inhibitory FactorMediatingMembrana Synovialis Capsulae ArticularisMemoryMiceMice MammalsMicrosatellite MarkersMicrosatellite RepeatsMicrosatellitesMigration Inhibition FactorMigration Inhibitory FactorModern ManMolecular InteractionMorbidityMorbidity - disease rateMouse StrainsMurineMusMΟPathogenicityPathologicPathologyPathway interactionsPatientsPgp1PhasePhenotypePlayPopulationProductionProtein IsoformsRNA SplicingReceptor ProteinRecurrent diseaseRefractoryRelapseRelapsed DiseaseRheumatoid ArthritisRisk-associated variantRoleSLESclerodermaSignal TransductionSignal Transduction SystemsSignalingSiteSplicingSymptomsSynoviaSynovial FluidSynovial MembraneSynovial jointSynovitisSynoviumSystemic Lupus ErythematosusSystemic Lupus ErythematousSystemic Lupus ErythmatosusT cell responseT memory cellT-CellsT-LymphocyteTestingTissuesTranscription Factor Proto-OncogeneTranscription factor genesUnited StatesVariantVariationVasculitisWorkantibody receptorarthriticarthropathicarthropathiesarthropathyarylpyruvate keto-enol tautomeraseautoimmune conditionautoimmune disorderautoimmunity diseasebiological signal transductionbiological therapeuticbiological treatmentbiologically based therapeuticsbiotherapeuticsbiotherapycardiovascular disordercell culturecell culturesclinical testcytokinedermatosclerosisdisseminated lupus erythematosusdrug-like chemicaldrug-like compounddrug-like moleculeeffective therapyeffective treatmentexperienceexperimentexperimental researchexperimental studyexperimentshuman migrationimmunopathologyinflamed synovial tissueinflamed synoviuminhibitorinsightjoint degenerationjoint degradationjoint destructionjoint disorderjoint tissue degenerationjuvenile arthritisjuvenile idiopathic arthritislife spanlifespanmemory T lymphocytemouse modelmurine modelnovelp-hydroxyphenylpyruvate tautomerasepathwayperipheral bloodphenylpyruvate tautomerasepolymorphismprogramspromoterpromotorprototypereceptorresearch clinical testingresponseresponse to therapyresponse to treatmentrheumatic arthritisrisk allelerisk generisk genotyperisk locirisk locusrisk variantsocial rolesynovial inflammationsystemic lupus erythematosistherapeutic responsetherapy responsethymus derived lymphocytetooltraffickingtranscription factortranslational impacttreatment responsetreatment responsivenessvasculitides
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PROJECT SUMMARY
Rheumatoid arthritis (RA) remains incurable despite biologic therapies. We previously identified a
functional promoter polymorphism in the gene for macrophage migration inhibitory factor (MIF) - a cytokine
our group first cloned, that is associated with erosive joint destruction in RA. MIF is known to regulate the
innate responseβ¦
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