grant

A novel mitochondria-to-lysosome stress signaling pathway in degenerative disease and aging

Organization UPSTATE MEDICAL UNIVERSITYLocation SYRACUSE, UNITED STATESPosted 1 Aug 2023Deadline 30 Apr 2028
NIHUS FederalResearch GrantFY20250-11 years oldAAC2AD dementiaAddressAffectAgingAlzheimer Type DementiaAlzheimer disease dementiaAlzheimer sclerosisAlzheimer syndromeAlzheimer'sAlzheimer's DiseaseAlzheimers DementiaAmino AcidsAmyotrophic Lateral SclerosisAmyotrophic Lateral Sclerosis Motor Neuron DiseaseAmyotrophic lateral sclerosis and frontotemporal degenerationAmyotrophic lateral sclerosis and frontotemporal dementiaArylamide Acetylase 2AtrophicAtrophyAutophagocytosisAutoregulationBiochemistryBioenergeticsBiologicalBiological ChemistryBiologyBody TissuesCarrier ProteinsCell AgingCell BodyCell Communication and SignalingCell DeathCell Death InductionCell FunctionCell Membrane PermeabilityCell PhysiologyCell ProcessCell SenescenceCell SignalingCell SurvivalCell ViabilityCellsCellular AgingCellular FunctionCellular PhysiologyCellular ProcessCellular SenescenceCerebroatrophic HyperammonemiaChildChild YouthChildren (0-21)Complex I DehydrogenaseCongestive CardiomyopathyCytosolDNA mutationDataDefectDegenerative DisorderDevelopmentDilated CardiomyopathyDiseaseDisorderDysfunctionElectron Transport Complex IEnergy ExpenditureEnergy MetabolismEnvironmentEnzyme GeneEnzymesFSHDFTD dementiaFTD/ALSFTLD/ALSFacioscapulohumeral AtrophyFacioscapulohumeral Muscular DystrophyFacioscapulohumeral Type Progressive Muscular DystrophyFasioscapulohumeral Muscular DystrophyFrontal Temporal DementiaFrontotemporal DementiaFrontotemporal Lobar Degeneration/Amyotrophic lateral sclerosisFunctional disorderGehrig's DiseaseGeneHomologGenesGeneticGenetic ChangeGenetic defectGenetic mutationGoalsH(+) PumpH+ PumpHomeostasisHomologHomologous GeneHomologueHumanImpairmentIntracellular Communication and SignalingIonsLandouzy Dejerine muscular dystrophyLandouzy-Dejerine DystrophyLeigh DiseaseLeigh SyndromeLou Gehrig DiseaseLysosomesMammalian CellMetabolic Protein DegradationMiceMice MammalsMitochondriaMitochondrial DiseasesMitochondrial DisordersMitochondrial ProteinsModelingModern ManMolecularMultienzyme ComplexesMultivesicular BodyMurineMusMuscle AtrophyMuscular AtrophyMutationN-Acetyltransferase 2NADH DH INADH Dehydrogenase Complex 1NADH Dehydrogenase INADH Q1 OxidoreductaseNADH dehydrogenase (ubiquinone)NADH-CoQ ReductaseNADH-Coenzyme Q ReductaseNADH-Ubiquinone OxidoreductaseNADH-Ubiquinone ReductaseNAT-2NAT2NAT2 geneNamesNuclearOrganellesOxidative PhosphorylationOxidative Phosphorylation PathwayParalysis AgitansParkinsonParkinson DiseasePathogenicityPathway interactionsPhenotypePhysiological HomeostasisPhysiopathologyPlayPrimary ParkinsonismPrimary Senile Degenerative DementiaProcessProductionProtein ImportProtein TurnoverProteinsProton PumpRegulatory Protein DegradationReplicative SenescenceRespiratory Complex IRett DisorderRett SyndromeRoleRotenone-Sensitive Mitochondrial NADH-Ubiquinone OxidoreductaseSignal PathwaySignal TransductionSignal Transduction SystemsSignalingSkeletal MuscleStressSubacute Necrotizing EncephalomyelitisSubacute Necrotizing EncephalomyelopathySubacute Necrotizing EncephalopathySubcellular ProcessSystemTestingTissuesTransgenic MiceTransport Protein GeneTransport ProteinsTransporter ProteinUbiquinone ReductaseV-ATPaseV-type ATPaseVacuoleVoluntary MuscleYeastsadult youthaging associatedaging associated diseaseaging associated disordersaging relatedaging related diseaseaging related disordersaminoacidamyotrophic lateral sclerosis with frontotemporal dementiaamyotrophic lateral sclerosis/FTLDamyotrophic lateral sclerosis/frontotemporal dementiaamyotrophic lateral sclerosis/ftdautophagybiochemical toolsbiochemistry toolsbiologicbiological signal transductioncell agecellular agecomplex 1 dehydrogenasedegenerative conditiondegenerative diseasedetection of nutrientdevelopmentaldiscover genesdisease associated with agingdisease of agingdisorder of agingdisorders associated with agingdisorders related to agingenzyme complexexperimentexperimental researchexperimental studyexperimentsfitnessfront temporal dementiafrontal lobe dementiafrontotemporal dementia-amyotrophic lateral sclerosisfrontotemporal lobar degeneration dementiafrontotemporal lobar dementiafrontotemporal lobar dementia amyotrophic lateral sclerosisfrontotemporal lobe degeneration associated with dementiagene discoverygenome mutationgenomic toolshallmarks of agingin vivokidslate endosomelife spanlifespanmembrane permeabilitymitochondrialmouse modelmurine modelmuscle breakdownmuscle degradationmuscle deteriorationmuscle lossmuscle wastingnamenamednamingnecrocytosisnovelnutrient sensingoverexpressoverexpressionpathophysiologypathwayperception of nutrientspillars of agingpostmitoticprimary degenerative dementiaprotein degradationreplicative agingsenile dementia of the Alzheimer typesocial rolestressorsuccesssynergismsynthetic lethal interactionsynthetic lethalitytraffickingtype 1 dehydrogenasevacuolar ATPasevacuolar H+-ATPasevacuolar membrane H(+)-ATPaseyoung adultyoung adult ageyoung adulthoodyoungster
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This application synergizes expertise from two groups, with one specialized in mitochondrial biology and
proteostatic signaling and the other in V-ATPase biochemistry and vacuolar/lysosomal biology. Mitochondria

are multifunctional organelles. In addition to their major role in ATP production, mitochondria are also involved

in other cellular…

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A novel mitochondria-to-lysosome stress signaling pathway in degenerative disease and aging — UPSTATE MEDICAL UNIVERSITY | Dev Procure