grant
Molecular and cellular mechanisms of spinocerebellar ataxia type 5
Organization OAKLAND UNIVERSITYLocation ROCHESTER, UNITED STATESPosted 1 Mar 2020Deadline 30 Jun 2028
NIHUS FederalResearch GrantFY2025Actin-Activated ATPaseActinsAffinityAllelesAllelomorphsAppendicular AtaxiasAtaxiaAtaxyBindingBiochemicalCell Communication and SignalingCell SignalingCellular MatrixCoordination ImpairmentCoupledCryo-electron MicroscopyCryoelectron MicroscopyCytoskeletal GeneCytoskeletal ProteinsCytoskeletal SystemCytoskeletonDNA Molecular BiologyDNA mutationDataDefectDegenerative Neurologic DisordersDendritesDevelopmentDrosophilaDrosophila genusDrosophila in proteinDrosophila inturned proteinDyssynergiaElectron CryomicroscopyFliesFundingFutureGait AtaxiaGenesGeneticGenetic ChangeGenetic defectGenetic mutationGoalsGrantImmune PrecipitationImmunoprecipitationImpairmentIn VitroIntracellular Communication and SignalingInvestigatorsKI miceKinasesKnock-in MouseKnowledgeLimb AtaxiaMass Photometry/Spectrum AnalysisMass SpectrometryMass SpectroscopyMass SpectrumMass Spectrum AnalysesMass Spectrum AnalysisMiceMice MammalsMissense MutationModelingMolecularMolecular BiologyMolecular InteractionMurineMusMutationMyosin ATPaseMyosin Adenosine TriphosphataseMyosin AdenosinetriphosphataseMyosinsN-terminalNH2-terminalNerve CellsNerve UnitNervous System Degenerative DiseasesNeural CellNeural Degenerative DiseasesNeural degenerative DisordersNeurocyteNeurodegenerative DiseasesNeurodegenerative DisordersNeurologic Degenerative ConditionsNeuronsPathogenesisPathway interactionsPhenotypePhosphatasesPhosphohydrolasesPhosphomonoesterasesPhosphoric Monoester HydrolasesPhosphorylationPhosphotransferase GenePhosphotransferasesPost-Transcriptional Gene SilencingProtein PhosphorylationProteinsPurkinje CellsPurkinje's CorpusclesRNA InterferenceRNA SilencingRNAiResearchResearch PersonnelResearchersRoleSequence-Specific Posttranscriptional Gene SilencingSignal TransductionSignal Transduction SystemsSignalingSpectrinSpinocerebellar Ataxia Type 5Spinocerebellar Ataxia-5StructureSystemTalentsTestingTrainingTransphosphorylasesTropomyosinUniversitiesWorkbeta Spectrinbiological signal transductioncerebellar Purkinje cellcryo-EMcryoEMcryogenic electron microscopydegenerative diseases of motor and sensory neuronsdegenerative neurological diseasesdevelopmentaldominant genetic mutationdominant mutationflyfruit flygene manipulationgenetic approachgenetic manipulationgenetic strategygenetically manipulategenetically perturbgenome mutationin vivoinsightintracellular skeletonknockin miceloss of functionmimeticsmissense single nucleotide polymorphismmissense single nucleotide variantmissense variantmutantneural cell bodyneurodegenerative illnessneuronalneuronal cell bodynew therapeutic approachnew therapeutic interventionnew therapeutic strategiesnew therapy approachesnew treatment approachnew treatment strategynext generationnovelnovel therapeutic approachnovel therapeutic interventionnovel therapeutic strategiesnovel therapy approachpathwayprotein functionsocial rolesomatherapeutic agent developmenttherapeutic developmentundergradundergraduateundergraduate studentβ-Spectrin
Description preview
β-III-spectrin is a key cytoskeletal protein that localizes to the soma and dendrites of cerebellar Purkinje
neurons, and is required for dendritic arborization and signaling. Dominant mutations in the SPTBN2 gene
encoding β-III-spectrin cause the neurodegenerative disorder spinocerebellar ataxia type 5 (SCA5). SCA5
causes degeneration of Purkinje…
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