grant
Regulation of SGK1-mediated Pathological Cardiac Hypertrophy by Non-Canonical ERAD
Organization UNIVERSITY OF ARIZONALocation TUCSON, UNITED STATESPosted 1 Dec 2024Deadline 30 Jun 2029
NIHUS FederalResearch GrantFY202620S Catalytic Proteasome20S Core Proteasome20S Proteasome20S ProteosomeAddressCardiacCardiac DiseasesCardiac DisordersCardiac Muscle CellsCardiac MyocytesCardiac OutputCardiocyteCardiovascular DiseasesCatalytic CoreCatalytic DomainCatalytic RegionCatalytic SiteCatalytic SubunitCell Communication and SignalingCell FunctionCell PhysiologyCell ProcessCell SignalingCellular FunctionCellular PhysiologyCellular ProcessChronicClinicalCommon Rat StrainsDevelopmentDysfunctionE3 LigaseE3 Ubiquitin LigaseEndoplasmic ReticulumEquilibriumErgastoplasmFaceFunctional disorderGeneralized GrowthGrowthHeartHeart DiseasesHeart HypertrophyHeart Muscle CellsHeart failureHeart myocyteHumanHypertensionHypertrophyImpairmentIn VitroIndividualInterventionIntracellular Communication and SignalingKinasesL-LysineLeft VentriclesLeft ventricular structureLysineMacropainMacroxyproteinaseMalignant CellMediatingMembraneMetabolic Protein DegradationMiceMice MammalsModern ManMolecularMulticatalytic ProteinaseMurineMusMuscle CellsMyocytesN-terminalNH2-terminalNeonatalOrganellesPathologicPathologyPhosphotransferase GenePhosphotransferasesPhysiopathologyPoint MutationProcessProsomeProteasomeProteasome Endopeptidase ComplexProtein BiosynthesisProtein TurnoverProteinsProteosomeRatRats MammalsRattusRegulationRegulatory Protein DegradationResistanceRibosomal Peptide BiosynthesisRibosomal Protein BiosynthesisRibosomal Protein SynthesisRisk FactorsRoleSGK1 proteinSerum-glucocorticoid-regulated kinase 1Sgk proteinSignal TransductionSignal Transduction SystemsSignalingSiteStimulusStudy of serumSubcellular ProcessTherapeuticTissue GrowthTransphosphorylasesUbiquitin Protein LigaseUbiquitin-Protein Ligase ComplexesUbiquitin-Protein Ligase E3Vascular Hypertensive DiseaseVascular Hypertensive DisorderVascular blood supplyVentricularWorkaberrant folded proteinaberrant folded proteinsabnormal folded proteinabnormal folded proteinsbalancebalance functionbiological signal transductionblood supplycancer cellcardiac failurecardiac functioncardiac hypertrophycardiomyocytecardiovascular disorderdecline in functiondecline in functional statusdevelopmentalexperimentexperimental researchexperimental studyexperimentsfacesfacialfunction of the heartfunctional declinefunctional status declineheart disorderheart functionheart outputhigh blood pressurehyperpiesiahyperpiesishypertensive diseasehypertensive disorderin vivoinnovateinnovationinnovativeinsightknock-downknockdownmembrane structuremisfolded proteinmisfolded proteinsmortalitymouse modelmulticatalytic endopeptidase complexmurine modelmutantontogenyoverexpressoverexpressionpathophysiologypressurepreventpreventingprotein degradationprotein foldingprotein homeostasisprotein synthesisproteostasisproteotoxic proteinproteotoxinresistantresponseserum and glucocorticoid-regulated kinasesocial roletherapeutic targettherapeutically effectivetoolubiquitin-protein ligasevascular supply
Description preview
Project Summary: Heart disease is the leading cause of mortality and is often preceded by pathological cardiac
hypertrophy due to chronic hypertension and sustained increases in cardiac afterload. While initially an adaptive
response to maintain cardiac output and systemic blood supply, pathological cardiac hypertrophy eventually
leads to a…
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