grant
C2 domain therapeutics for muscular dystrophy
Organization UNIVERSITY OF MARYLAND BALTIMORELocation BALTIMORE, UNITED STATESPosted 30 Jul 2024Deadline 30 Jun 2029
NIHUS FederalResearch GrantFY2025Adverse effectsAffectAmericanAmino AcidsAssayBindingBioassayBiological AssayC 2aC-terminalC2 DomainC2aCalcium Ion SignalingCalcium SignalingCell Communication and SignalingCell SignalingCessation of lifeChimeraChimera organismClinical TreatmentClinical TrialsCodeCoding SystemCollaborationsCompensationComplexCytoplasmDNA RecombinationDNA TherapyDNA mutationDYSFDYSF geneDataDeathDefectDiseaseDisorderDoseEngineeringEventFER1L1FailureFamily memberFrequenciesGene ProteinsGene Transfer ClinicalGenesGenetic ChangeGenetic InterventionGenetic RecombinationGenetic defectGenetic mutationGoalsHeterozygoteIn VitroIndividualInjuryIntracellular Communication and SignalingLGMD2BLearningLengthLimb girdle muscular dystrophy 2B (autosomal recessive)Limb-Girdle Muscular DystrophiesLinkMeasuresMediatingMembraneMiceMice MammalsMissense MutationMiyoshi myopathyMolecular InteractionMurineMusMuscleMuscle CellsMuscle DiseaseMuscle DisordersMuscle TissueMuscular DiseasesMuscular DystrophiesMutateMutationMyocytesMyodystrophicaMyodystrophyMyopathic ConditionsMyopathic Diseases and SyndromesMyopathic disease or syndromeMyopathyN-terminalNH2-terminalNeuromuscular DiseasesNonsense CodonORFsOpen Reading FramesPKC(alpha)PKCAPKCαPRKCAPRKCA genePathogenicityPathologicPathologyPatientsPhenotypePhosphatidesPhospholipidsPhysiologicPhysiologicalPlayPoint MutationPremature Stop CodonPreparationProcessPropertyProtein Coding RegionProtein Gene ProductsProtein Kinase C AlphaProtein Kinase C αProtein Kinase CalphaProteinsRNA SplicingRecombinationReportingRoleRyR1Signal TransductionSignal Transduction SystemsSignalingSkeletal MuscleSpecificitySplicingStriated MusclesStructureTestingTherapeuticVariantVariationViralVoluntary MuscleWorkaminoacidbiological signal transductionchimerasclinical interventionclinical therapycomplement 2acomplement C2acomplement C2a fragmentdesigndesigningdysferlindysferlinopathic diseasedysferlinopathiesdysferlinopathy diseaseeffective therapyeffective treatmentexperimentexperimental researchexperimental studyexperimentsfer-1-like family membergene nullgene repairgene repair therapygene therapygene-based therapygenetic therapygenome mutationgenomic therapyheterozygosityimprovedin vitro Assayin vivoinjuriesinsightlimb-girdle muscular weakness and atrophylimb-girdle syndromemembrane structuremissense single nucleotide polymorphismmissense single nucleotide variantmissense variantmuscle dystrophymuscularmuscular disordermutantmyoneural disordermyopathic limb-girdle syndromeneuromuscular degenerative disorderneuromuscular disordernovelnull mutationpreparationsprotein kinase Cαrepairrepairedskeletalsocial roletransduction efficiencytrial regimentrial treatmentvector
Description preview
Mutations in the dysferlin gene (DYSF) cause Limb Girdle Muscular Dystrophy Type 2B (LGMD 2B) and
Miyoshi Myopathy (MMD1) and affect ~1:100,000 individuals worldwide. Dysferlin is comprised of ferlin and
dysferlin domains flanked by C2 domains and it accumulates in t-tubule membranes (TTs) at triad junctions
(TJs). Our labs have been collaborating…
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