grant
Laminin protein therapy for the treatment of Laminin-alpha2 deficient congenital muscular dystrophy
Organization UNIVERSITY OF NEVADA RENOLocation RENO, UNITED STATESPosted 1 Apr 2024Deadline 31 Mar 2029
NIHUS FederalResearch GrantFY202621+ years oldAdhesionsAdultAdult HumanAssayAxonBasal laminaBasement membraneBioassayBiologicalBiological AssayBirthCardiotoxinCell Communication and SignalingCell LineCell SignalingCell-Extracellular MatrixCellLineCobra CardiotoxinComplexCongenital muscular dystrophy 1ACongenital muscular dystrophy type 1ADNA mutationDataDefectDevelopmentDiameterDirect Lytic FactorsDisease ProgressionDistalDucheneDuchenneDuchenne muscular dystrophyDuchenne-Griesinger syndromeECMEllis-van Creveld (EvC) syndromeEmbryoEmbryonicEmbryonic Muscle CellsEngraftmentEnteral FeedingExhibitsExtracellular MatrixExtracellular Matrix ProteinsGeneralized GrowthGenesGenetic ChangeGenetic defectGenetic mutationGlycoprotein GP-2GoalsGrowthHumanImmune responseImmunohistochemistryImmunohistochemistry Cell/TissueImmunohistochemistry Staining MethodImpairmentIntracellular Communication and SignalingIsoformsKidneyKidney Urinary SystemKyphosisKyphosis deformity of spineLamininLaminin-α2Laminin-α2-related Congenital Muscular DystrophyLifeLife ExpectancyMDC1AMeasuresMerosin deficient congenital muscular dystrophyMerosin-Deficient Congenital Muscular Dystrophy 1AMerosin-Deficient Congenital Muscular Dystrophy type 1AMiceMice MammalsMicroscopyModelingModern ManMolecularMotor CellMotor NeuronsMurineMusMuscleMuscle AtrophyMuscle CellsMuscle DevelopmentMuscle DiseaseMuscle DisordersMuscle TissueMuscle WeaknessMuscle functionMuscle satellite cellMuscular AtrophyMuscular DevelopmentMuscular DiseasesMuscular WeaknessMutationMyelinMyoblastsMyocytesMyopathic ConditionsMyopathic Diseases and SyndromesMyopathic disease or syndromeMyopathyNerveNerve ConductionNeural ConductionNeurilemma CellNeurilemmal CellNeuromuscular DiseasesOnset of illnessParturitionPathologyPatientsPeripheral NervesPlayPreclinical dataPrecursor Muscle CellsProtein IsoformsProtein Replacement TherapyProteinsPseudohypertrophic Muscular DystrophyReceptor CellRecombinantsResolutionRespiratory InsufficiencyRoleSchwann CellsSignal PathwaySignal TransductionSignal Transduction SystemsSignalingSkeletal MuscleSpinal Nerve RootsSpinal RootsSpinal nerve root structureStrains Cell LinesTestingThickThicknessTissue GrowthTransmission Electron MicroscopyVentilatorVoluntary MuscleX-linked dilated cardiomyopathyX-linked muscular dystrophyX-linked recessive muscular dystrophyadulthoodbenign X-linked recessive muscular dystrophybiologicbiological signal transductionbiomarker identificationcanine animal modelcanine modelchildhood pseudohypertrophic muscular dystrophyclassic X-linked recessive muscular dystrophycongenital muscular dystrophycultured cell linecurative interventioncurative therapeuticcurative therapycurative treatmentsdevelopmentaldigitaldisease onsetdisorder onsetdog modeleffective therapyeffective treatmententeric feedingenzyme replacement therapyenzyme replacement treatmentfeeding tubefunctional lossfunctional restorationgastric feedinggenome mutationhost responseidentification of biomarkersidentification of new biomarkersimmune system responseimmunoresponseimprovedin vitro Assayinsightlaminin alpha 2marker identificationmild X-linked recessive muscular dystrophymotoneuronmouse modelmurine modelmuscle breakdownmuscle degradationmuscle deteriorationmuscle fiber repairmuscle lossmuscle regenerationmuscle repairmuscle strengthmuscle structuremuscle tissue repairmuscle wastingmuscularmuscular disordermuscular repairmuscular structuremyelinationmyogenesismyoneural disorderneuromuscular degenerative disorderneuromuscular disorderneuromuscular functionontogenypreclinical findingspreclinical informationprematureprematurityprogramsprogressive muscular dystrophy of childhoodpseudohypertrophic adult muscular dystrophypseudohypertrophic muscular paralysisrenalrepairrepair functionrepairedreparative functionresolutionsrestore functionrestore functionalityrestore lost functionsatellite cellskeletal muscle growthsocial rolesuperresolution microscopytube feedingyounger age
Description preview
Project Summary
Laminin-α2-related Congenital Muscular Dystrophy (LAMA2-CMD), also known as Merosin Deficient
Congenital Muscular Dystrophy type 1A (MDC1A), is a devastating neuromuscular disease characterized by
progressive muscle weakness from birth. LAMA2-CMD is caused by mutations in the LAMA2 gene, which results
in the loss of the Laminin-α2…
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