grant
Defining the cardiomyocyte microdomain signaling landscape in cardiac hypertrophy
Organization UNIVERSITY OF MICHIGAN AT ANN ARBORLocation ANN ARBOR, UNITED STATESPosted 1 Apr 2023Deadline 31 Mar 2028
NIHUS FederalResearch GrantFY202621+ years oldATP-protein phosphotransferaseActive OxygenAcylationAdultAdult HumanAgeAmericanAngIIAngiotensin IIAngiotensin ReceptorArchitectureArrhythmiaAutoregulationBiochemicalBiologicalBiosensorBontoxilysinBotulinBotulinum ToxinsCaM KIICaM PK IICaM kinase IICaMKIICardiacCardiac ArrhythmiaCardiac DiseasesCardiac DisordersCardiac Muscle CellsCardiac MyocytesCardiocyteCardiovascular DiseasesCause of DeathCell Communication and SignalingCell Membrane Lipid RaftsCell SignalingCessation of lifeChemical FractionationClostridium botulinum ToxinsComplexCysteineDNA mutationDataDeathDevelopmentDysfunctionEconomic BurdenEngineering / ArchitectureEnzyme GeneEnzymesEventExhibitsFRACNFamilyFatty AcidsFractionationFractionation RadiotherapyFunctional disorderGTPGeneralized GrowthGenerationsGenetic ChangeGenetic defectGenetic mutationGolgiGolgi ApparatusGolgi ComplexGrowthGuanosine TriphosphateHalf-CystineHeart ArrhythmiasHeart DiseasesHeart HypertrophyHeart Muscle CellsHeart failureHeart myocyteHomeostasisHumanHypertrophyInfusionInfusion proceduresIntercalated discIntracellular Communication and SignalingIntracellular MembranesKinase Family GeneKnock-inL-CysteineLateralLipidsMediatingMembraneMembrane MicrodomainsMiceMice MammalsModern ManModificationMolecularMonomeric G-ProteinsMonomeric GTP-Binding ProteinsMurineMusMuscle CellsMutationMyocardialMyocardiumMyocytesNADPH OxidaseOxidation-ReductionOxidative StressOxygen RadicalsPalmitic Acylation SitePalmitoylation SitePathogenesisPathogenicityPathway interactionsPhenotypePhosphorylationPhysiologicPhysiologicalPhysiological HomeostasisPhysiopathologyPrevalencePro-OxidantsProductionProtein KinaseProtein PhosphorylationProteinsProteomicsPublic HealthReactive Oxygen SpeciesRedoxRegulationReportingRoleSarcolemmaSignal PathwaySignal TransductionSignal Transduction SystemsSignalingSmall G-ProteinsSmall GTPasesSphingolipid MicrodomainsSphingolipid-Cholesterol RaftsTC-25 GTP-Binding ProteinTestingTissue GrowthTransgenic MiceUnited Statesadulthoodagesbiologicbiological sensorbiological signal transductionbotulinum neurotoxincalcium-dependent CaM kinase IIcalmodulin-dependent protein kinase IIcardiac failurecardiac functioncardiac hypertrophycardiac musclecardiomyocytecardioprotectantcardioprotectioncardioprotectivecardiovascular disordercell typeclinical relevanceclinically relevantdevelopmentalefficacious therapyefficacious treatmentexperimentexperimental researchexperimental studyexperimentsfunction of the heartgenome mutationglycogen synthase a kinaseheart disorderheart functionheart musclehydroxyalkyl protein kinasein vivoinduced Creinducible Creinfusionsknockinlipid raftmembrane structuremortalitymouse modelmurine modelmutantnovelontogenyoverexpressoverexpressionoxidation reduction reactionpalmitoylationpathophysiologypathwayphosphorylase b kinase kinasepreservationprotein functionrac1 GTP-Binding Proteinrac1 Proteinras-Related C3 Botulinum Toxin Substrate 1responserhosocial rolespatial and temporalspatial temporalspatiotemporal
Description preview
Abstract
Heart disease is the leading cause of death globally and poses an enormous public health and economic
burden. In the United States, prevalence and mortality due to heart failure have even increased in recent years,
underscoring the need for a greater understanding of pathophysiological signaling mechanisms that underlie
cardiac…
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