2025
Cornuside alleviates cognitive impairments induced by Aβ1−42 through attenuating NLRP3-mediated neurotoxicity by promoting mitophagy
Zhou F, Lian W, Yuan X, Wang Z, Xia C, Yan Y, Wang W, Tong Z, Cheng Y, Xu J, He J, Zhang W. Cornuside alleviates cognitive impairments induced by Aβ1−42 through attenuating NLRP3-mediated neurotoxicity by promoting mitophagy. Alzheimer's Research & Therapy 2025, 17: 47. PMID: 39972387, PMCID: PMC11837312, DOI: 10.1186/s13195-025-01695-w.Peer-Reviewed Original ResearchConceptsMitochondrial functionMitochondrial membrane potential depolarizationNLRP3 inflammasome activationInflammasome activationAlzheimer's diseasePromotion of mitophagyAnti-AD candidateBNIP3 pathwayFormation of autophagosomesDamaged mitochondriaProgressive neurodegenerative disorderProduction of ROSMitophagy fluxOxidative phosphorylationMitophagyMembrane potential depolarizationPINK1/Parkin signalingIncreased colocalizationMitochondrial dysfunctionNLRP3 inflammasomeAD miceSynaptic damageEt ZuccCaspase-1Neurodegenerative disorders
2019
Mitochondrial MsrB2 serves as a switch and transducer for mitophagy
Lee SH, Lee S, Du J, Jain K, Ding M, Kadado AJ, Atteya G, Jaji Z, Tyagi T, Kim W, Herzog RI, Patel A, Ionescu CN, Martin KA, Hwa J. Mitochondrial MsrB2 serves as a switch and transducer for mitophagy. EMBO Molecular Medicine 2019, 11: emmm201910409. PMID: 31282614, PMCID: PMC6685081, DOI: 10.15252/emmm.201910409.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlood PlateletsCell LineDiabetes MellitusFemaleHumansMethionine Sulfoxide ReductasesMice, Inbred C57BLMice, KnockoutMicrofilament ProteinsMicrotubule-Associated ProteinsMitochondriaMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMitophagyMutationOxidation-ReductionOxidative StressParkinson DiseaseSignal TransductionUbiquitin-Protein LigasesUbiquitinationConceptsReduced mitophagyOxidative stress-induced mitophagyNovel regulatory mechanismStress-induced mitophagyLC3 interactionMitochondrial matrixDamaged mitochondriaMsrB2Reactive oxygen speciesRegulatory mechanismsMethionine oxidationMitophagyMitochondriaPlatelet apoptosisOxygen speciesPlatelet-specific knockoutApoptosisPathophysiological importanceExpressionImportant roleUbiquitinationParkin mutationsParkinSpeciesLC3
2015
The PINK1-PARKIN Mitochondrial Ubiquitylation Pathway Drives a Program of OPTN/NDP52 Recruitment and TBK1 Activation to Promote Mitophagy
Heo JM, Ordureau A, Paulo JA, Rinehart J, Harper JW. The PINK1-PARKIN Mitochondrial Ubiquitylation Pathway Drives a Program of OPTN/NDP52 Recruitment and TBK1 Activation to Promote Mitophagy. Molecular Cell 2015, 60: 7-20. PMID: 26365381, PMCID: PMC4592482, DOI: 10.1016/j.molcel.2015.08.016.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingCell Cycle ProteinsHeLa CellsHumansMembrane Transport ProteinsMitochondriaMitophagyNuclear ProteinsPhosphorylationProtein KinasesProtein Serine-Threonine KinasesProteomicsSequestosome-1 ProteinTranscription Factor TFIIIAUbiquitin-Protein LigasesUbiquitinationConceptsUbiquitin chainsEfficient mitophagyTBK1 activationPINK1-Parkin pathwayUbiquitylation pathwayAdaptor recruitmentCellular homeostasisMitochondrial retentionTBK1 kinaseDamaged mitochondriaChain bindingMitophagyHeLa cellsMitochondriaPhosphorylationNDP52Positive feedback mechanismPathwayOPTNRecruitmentActivationAmyotrophic lateral sclerosisAssemblyS473Kinase
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