grant

The role N-terminal acetylation in dilated cardiomyopathy and associated arrhythmia

Organization BOSTON CHILDREN'S HOSPITALLocation BOSTON, UNITED STATESPosted 3 Aug 2023Deadline 30 Apr 2027
NIHUS FederalResearch GrantFY2026ASDAblationAcetylationAcetyltransferaseAction PotentialsAffectAnimal ModelAnimal Models and Related StudiesArrhythmiaAutismAutistic DisorderAutoregulationBiologic ModelsBiological ModelsCalciumCardiacCardiac AbnormalitiesCardiac ArrhythmiaCardiac DiseasesCardiac DisordersCardiac MalformationCardiac Muscle CellsCardiac MyocytesCardiocyteCardiomyopathiesCardiovascular DiseasesCatalytic CoreCatalytic DomainCatalytic RegionCatalytic SiteCatalytic SubunitCharacteristicsComplexCongestive CardiomyopathyDNA mutationDataDevelopmental DelayDevelopmental Delay DisordersDilated CardiomyopathyDiseaseDisorderDysfunctionEarly Infantile AutismElectrophysiologyElectrophysiology (science)FamilyFamily memberFibrosisFunctional disorderGenetic ChangeGenetic PredispositionGenetic Predisposition to DiseaseGenetic SusceptibilityGenetic defectGenetic mutationGenetic propensityHeartHeart AbnormalitiesHeart ArrhythmiasHeart DiseasesHeart MalformationHeart Muscle CellsHeart failureHeart myocyteHomeostasisHumanImpairmentIndividualInfantile AutismInherited PredispositionInherited SusceptibilityIon ChannelIonic ChannelsIonsK channelK elementKO miceKanner's SyndromeKnock-out MiceKnockout MiceLearning DisabilitiesLearning disabilityMediatingMembrane ChannelsModel SystemModelingModern ManModificationMorbidityMutationMyocardialMyocardial DiseasesMyocardial DisorderMyocardial depressionMyocardial dysfunctionMyocardiopathiesN-terminalNH2-terminalNa elementNeurophysiology / ElectrophysiologyNull MousePatientsPedigreePhenotypePhysiologicPhysiologicalPhysiological HomeostasisPhysiopathologyPost-Translational Modification Protein/Amino Acid BiochemistryPost-Translational ModificationsPost-Translational Protein ModificationPost-Translational Protein ProcessingPosttranslational ModificationsPosttranslational Protein ProcessingPotassiumPotassium ChannelPotassium Ion ChannelsProtein ModificationProteinsProteomeProteomicsRecurrenceRecurrentRiskRoleSodiumSodium ChannelSodium Ion ChannelsSpecific Child Development DisordersStructureSudden DeathTestingVentricular ArrhythmiaVentricular Dysfunctionabnormal heart developmentautism spectral disorderautism spectrum disorderautistic spectrum disorderboyscardiac dysfunctioncardiac failurecardiac functioncardiac myocytes differentiated from induced pluripotent stem cellcardiac rhythmcardiomyocytecardiovascular disorderclinical phenotypecongenital cardiac abnormalitycongenital cardiac anomaliescongenital cardiac diseasecongenital cardiac disordercongenital cardiac malformationcongenital heart abnormalitycongenital heart anomalycongenital heart diseasecongenital heart disordercongenital heart malformationelectrophysiologicalfemale patientsfunction of the heartgenetic pedigreegenetic vulnerabilitygenetically predisposedgenome mutationheart disorderheart dysfunctionheart functionheart rhythmiPSiPS cell derived cardiomyocytesiPSCiPSC derived cardiomyocytesiPSCsimprovedinduced pluripotent cellinduced pluripotent stem cellinduced pluripotent stem cell derived cardiac myocytesinduced pluripotent stem cell derived cardiomyocytesinducible pluripotent cellinducible pluripotent stem cellinducible pluripotent stem cell derived cardiac myocytesinducible pluripotent stem cells derived cardiomyocytesinsightkindredmalemodel of animalmortalitymouse modelmurine modelmyocardium diseasemyocardium disordernoveloverexpressoverexpressionpathophysiologypatients being femalepatients being womenpatients who are femalepedigree structurepressureprogenitor cell modelprogenitor modelprotein complexrisk stratificationsocial rolestem and progenitor cell modelstem cell based modelstem cell derived modelstem cell modelstratify risktherapeutic agent developmenttherapeutic developmentwomen patients
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PROJECT SUMMARY
Cardiomyopathy and heart failure are leading causes of morbidity and mortality world-wide. In

addition to ventricular dysfunction, heart-failure associated ventricular arrhythmias cause sudden

death with few disease-modifying therapies. Changes in myocardial conduction, increased fibrosis,

alterations of ion channel…

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The role N-terminal acetylation in dilated cardiomyopathy and associated arrhythmia — BOSTON CHILDREN'S HOSPITAL | UNITE | Dev Procure