grant
Role of SLC46A3 in the pathogenesis of inflammatory bowel disease
Organization UNIV OF MASSACHUSETTS MED SCH WORCESTERLocation WORCESTER, UNITED STATESPosted 1 Apr 2026Deadline 31 Mar 2028
NIHUS FederalResearch GrantFY202621+ years oldAcetylmuramyl-Alanyl-IsoglutamineAdultAdult HumanAffectAgonistAnimalsAutomobile DrivingAutophagocytosisAutoregulationB blood cellsB cellB cellsB-CellsB-LymphocytesB-cellBacteriaBone MarrowBone Marrow Reticuloendothelial SystemC rodentiumC. rodentiumCarrier ProteinsCausalityCell BodyCell Communication and SignalingCell LineCell SignalingCell WallCellLineCellsChemistryChronicCitrobacter freundii Biotype 4280Citrobacter rodentiumClinicalColitisColonCommunicationComplexCrohn diseaseCrohn'sCrohn's diseaseCrohn's disorderCytosolDNA mutationDataDiseaseDisease ProgressionDisorderDrosophilaDrosophila genusEpithelial CellsEpitheliumEtiologyExhibitsExtracellular Signal-Regulated Kinase GeneFamilyFutureGI microbiomeGI microbiotaGastrointestinal DiseasesGastrointestinal microbiotaGenesGenetic ChangeGenetic PolymorphismGenetic defectGenetic mutationGenetic studyGoalsGoblet CellsGranulomatous EnteritisGut EpitheliumHomeostasisHumanImmuneImmunesImmunologic ReceptorsImmunological ReceptorsImpairmentInfectionInflammationInflammatoryInflammatory Bowel DiseasesInflammatory Bowel DisorderInflammatory ResponseInnate Immune SystemInsectaInsectsInsects InvertebratesIntestinalIntestinesIntracellular Communication and SignalingInvestigationKO miceKinasesKnock-out MiceKnockout MiceLinkLiteratureMAP Kinase GeneMAPKMacrophageMammaliaMammalsMediatingMiceMice MammalsMitogen-Activated Protein Kinase GeneModern ManMolecularMuramyl DipeptideMureinMurineMusMutationMyeloid CellsMφNull MousePathogenesisPathologyPathway interactionsPatientsPeptidoglycanPhenotypePhosphotransferase GenePhosphotransferasesPhysiologicPhysiologicalPhysiological HomeostasisPredispositionPrevalenceProductionProtein Kinase InteractionReceptor ProteinReceptor-Interacting ProteinRegulationReportingResearchRiskRoleRouteSignal TransductionSignal Transduction SystemsSignalingSkinSodium Dextran SulfateStrains Cell LinesSusceptibilityTherapeuticTherapeutic InterventionTransphosphorylasesTransport Protein GeneTransport ProteinsTransporter Proteinadulthoodalpha-Defensinsanti-microbial peptideautophagybiological signal transductionbowelcausationcolitis mouse modelcolitis murine modelcultured cell linecytokinedigestive tract microbiomedisease causationdrivingdysbacteriosisdysbiosisdysbioticeleocolitisenteric microbial communityenteric microbiomeenteric microbiotafruit flygastrointestinal disordergastrointestinal epitheliumgastrointestinal microbial floragastrointestinal microbiomegene interactiongenome mutationgut communitygut floragut homeostasisgut microbe communitygut microbial communitygut microbial compositiongut microbial consortiagut microbiomegut microbiotagut microbioticgut microfloragut-associated microbiomehost microbiomeimmune receptorin vivoinflammatory disease of the intestineinflammatory disorder of the intestineintervention therapyintestinal autoinflammationintestinal barrierintestinal biomeintestinal epitheliumintestinal floraintestinal microbiomeintestinal microbiotaintestinal microfloraintestinal mucosal barrierintestinal tract microflorakeratinocyteloss of functionmicrobialmicrobial imbalancemicrobiomemouse colitismouse modelmurine colitismurine modelpathwaypolymorphismreceptorregional enteritissensorsocial rolesolutetargeted drug therapytargeted drug treatmentstargeted therapeutictargeted therapeutic agentstargeted therapytargeted treatmentuptakeα-Defensins
Description preview
Inflammatory bowel diseases (IBD), including Crohn’s disease (CD), remain a significant
clinical challenge with increasing prevalence, affecting millions worldwide despite recent
therapeutic advances. Loss-of-function polymorphisms in the Nod2 gene are strongly
associated with CD, which has long created a conundrum as NOD2 is a cytosolic innate…
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