grant
Regulation and impact of shortened TDP43 isoforms in FTD and ALS
Organization UNIVERSITY OF MICHIGAN AT ANN ARBORLocation ANN ARBOR, UNITED STATESPosted 1 Dec 2019Deadline 31 Aug 2029
NIHUS FederalResearch GrantFY2025AddressAffectAlternate SplicingAlternative RNA SplicingAlternative SplicingAmyotrophic Lateral SclerosisAmyotrophic Lateral Sclerosis Motor Neuron DiseaseAmyotrophic lateral sclerosis and frontotemporal degenerationAmyotrophic lateral sclerosis and frontotemporal dementiaAutopsyAutoregulationCell DifferentiationCell Differentiation processCollaborationsCytoplasmDNADegenerative DisorderDeoxyribonucleic AcidDepositDepositionDiseaseDisorderElementsEventExhibitsFTD/ALSFTLD/ALSFrontotemporal Lobar Degeneration/Amyotrophic lateral sclerosisFutureGehrig's DiseaseGene TranscriptionGenetic CodeGenetic TranscriptionHomeostasisHumanInclusion Body MyositisInvestigationIsoformsLabelLengthLou Gehrig DiseaseMediatingModelingModern ManMolecularMotor CellMotor NeuronsMuscle CellsMyocytesNerve CellsNerve DegenerationNerve UnitNeural CellNeurocyteNeuron DegenerationNeuronsNon-Polyadenylated RNAPathogenesisPathologicPathologyPathway interactionsPhysiologicPhysiologicalPhysiological HomeostasisProtein IsoformsProteinsProteomicsRNARNA DecayRNA ExpressionRNA Gene ProductsRNA SplicingRNA-Binding ProteinsRegulationResponse ElementsRibonucleic AcidSpinalSplicingTAR DNA binding protein 43 kDa pathologyTAR DNA binding protein 43 pathologyTAR DNA binding protein of 43 proteinopathyTAR DNA-binding protein 43TDP-43TDP-43 aggregateTDP-43 aggregationTDP43TDP43 aggregateTDP43 aggregationTDP43 associated neurodegenerationTDP43 associated neurodegenerative diseaseTDP43 associated pathologiesTDP43 induced neurodegenerationTDP43 neurodegenerationTDP43 neurodegenerative diseaseTDP43 neuropathologyTDP43 pathogenesisTDP43 pathologyTDP43 proteinopathyTDP43 related neurodegenerationTDP43 related pathologyTestingTrans active response DNA binding protein 43 pathologyTrans active response DNA binding protein of 43 kDa proteinopathyTranscriptionVariantVariationVisualizationamyotrophic lateral sclerosis with frontotemporal dementiaamyotrophic lateral sclerosis/FTLDamyotrophic lateral sclerosis/frontotemporal dementiaamyotrophic lateral sclerosis/ftdbiological adaptation to stresscell typecellular differentiationdegenerative conditiondegenerative diseaseexperimentexperimental researchexperimental studyexperimentsfrontotemporal dementia-amyotrophic lateral sclerosisfrontotemporal lobar dementia amyotrophic lateral sclerosishiPSChuman iPShuman iPSChuman induced pluripotent cellhuman induced pluripotent stem cellshuman inducible pluripotent stem cellshuman inducible stem cellshuman tissueinclusion-body myosytisinduced human pluripotent stem cellsloss of functionmotoneuronnecropsyneural degenerationneurodegenerationneurodegenerativeneurological degenerationneuronalneuronal degenerationnovelpathwaypostmortemprotein TDP-43protein TDP43reaction; crisisspatial RNA sequencingspatial gene expression analysisspatial gene expression profilingspatial resolved transcriptome sequencingspatial transcriptome analysisspatial transcriptome profilingspatial transcriptome sequencingspatial transcriptomicsspatially resolved transcriptomicsspatio transcriptomicsstress responsestress; reactiontraffickingtrans active response DNA binding protein 43 kDa pathologytrans active response DNA binding protein 43 proteinopathy
Description preview
ABSTRACT
Mislocalization of the transactive response element DNA/RNA binding protein of 43 kDa (TDP43) is a signature
event in an increasing number of degenerative diseases, including amyotrophic lateral sclerosis (ALS),
frontotemporal lobar degeneration (FTLD), and inclusion body myositis (IBM). Despite this, however, the
origins of TDP43…
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