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 TransductionUbiquitinationUbiquitin-Protein LigasesConceptsReduced mitophagyOxidative stress-induced mitophagyNovel regulatory mechanismStress-induced mitophagyLC3 interactionMitochondrial matrixDamaged mitochondriaMsrB2Reactive oxygen speciesRegulatory mechanismsMethionine oxidationMitophagyMitochondriaPlatelet apoptosisOxygen speciesPlatelet-specific knockoutApoptosisPathophysiological importanceExpressionImportant roleUbiquitinationParkin mutationsParkinSpeciesLC3
2016
Amelioration of ER stress by 4-phenylbutyric acid reduces chronic hypoxia induced cardiac damage and improves hypoxic tolerance through upregulation of HIF-1α
Jain K, Suryakumar G, Ganju L, Singh SB. Amelioration of ER stress by 4-phenylbutyric acid reduces chronic hypoxia induced cardiac damage and improves hypoxic tolerance through upregulation of HIF-1α. Vascular Pharmacology 2016, 83: 36-46. PMID: 27058435, DOI: 10.1016/j.vph.2016.03.004.Peer-Reviewed Original ResearchMeSH KeywordsAltitudeAnimalsApoptosisApoptosis Regulatory ProteinsChronic DiseaseCytoprotectionDisease Models, AnimalEndoplasmic Reticulum StressHypertrophy, Right VentricularHypoxiaHypoxia-Inducible Factor 1, alpha SubunitMaleMolecular ChaperonesMyocardiumOxidative StressPhenylbutyratesProtein CarbonylationProteolysisRats, Sprague-DawleySignal TransductionTime FactorsUnfolded Protein ResponseUp-RegulationConceptsChronic hypoxiaHIF-1αCardiac damageUnfolded protein responseER stressHypoxic toleranceRight ventricular enlargementExposure of ratsHypoxia-inducible factor-1ER stress modulationEndoplasmic reticulum stressInducible factor-1Ventricular enlargementCardiac injuryCardioprotective actionCardiovascular diseaseCardiac hypertrophyMarked upregulationActivation of UPRUnderlying causeUPR markersHypoxiaReticulum stressConcomitant suppressionFactor 1