2023
Contributions of circadian clock genes to cell survival in fibroblast models of lithium-responsive bipolar disorder
Mishra H, Wei H, Rohr K, Ko I, Nievergelt C, Maihofer A, Shilling P, Alda M, Berrettini W, Brennand K, Calabrese J, Coryell W, Frye M, Gage F, Gershon E, McInnis M, Nurnberger J, Oedegaard K, Zandi P, Kelsoe J, McCarthy M. Contributions of circadian clock genes to cell survival in fibroblast models of lithium-responsive bipolar disorder. European Neuropsychopharmacology 2023, 74: 1-14. PMID: 37126998, PMCID: PMC11801370, DOI: 10.1016/j.euroneuro.2023.04.009.Peer-Reviewed Original ResearchConceptsCell survival genesCircadian clockSurvival genesCell survivalCircadian clock genesCircadian rhythmGenetic variationClock genesKnockdown studiesCaspase activityCell deathMolecular pathwaysPrimary fibroblastsCellular modelGenesMouse fibroblastsFibroblast modelApoptosisStaurosporinePER1FibroblastsOpposite mannerLithium responsivenessDistinct patternsClock
2019
Vitamin E Prevents ΔN-Bcl-xL-associate Mitochondrial Dysfunction in Primary Hippocampal Neurons (P14-024-19)
Park H, Mnatsakanyan N, Broman K, Jonas E. Vitamin E Prevents ΔN-Bcl-xL-associate Mitochondrial Dysfunction in Primary Hippocampal Neurons (P14-024-19). Current Developments In Nutrition 2019, 3: nzz052.p14-024-19. PMCID: PMC6574370, DOI: 10.1093/cdn/nzz052.p14-024-19.Peer-Reviewed Original ResearchBcl-xL.Bcl-xLPrimary hippocampal neuronsMitochondrial dysfunctionRedox statusBcl-xL protein levelsCaspase-dependent cleavageAnti-apoptotic Bcl-xLMitochondrial redox statusPro-survival proteinsNeuronal deathMitochondrial oxidative stressHippocampal neuronsOxidative stressReactive oxygen species formationMitochondrial membraneCaspase activitySubsequent oxidative stressMitochondrial potentialMitochondrial functionNeuronal energy metabolismOxygen species formationDependent cleavageOxidative stress productionEnergy metabolism
2013
Growth Factor Receptor-Bound Protein 2 Promotes Autophagic Removal of Amyloid-β Protein Precursor Intracellular Domain Overload in Neuronal Cells
Roy K, Raychaudhuri M, Chakrabarti O, Mukhopadhyay D. Growth Factor Receptor-Bound Protein 2 Promotes Autophagic Removal of Amyloid-β Protein Precursor Intracellular Domain Overload in Neuronal Cells. Journal Of Alzheimer’s Disease 2013, 38: 881-895. PMID: 24100123, DOI: 10.3233/jad-130929.Peer-Reviewed Original ResearchConceptsAmyloid-β protein precursor intracellular domainRole of Grb2Dynamin-independent mannerTypes of vesiclesAutophagic removalApoptosis pointsGrowth factor receptorIntracellular domainVesicle accumulationCaspase activityDisease brainNeuronal cellsAD cell modelGrb2Independent mannerFactor receptorVesiclesAutophagosomesExcess conditionsAlzheimer's disease brainProtein overloadStudy unravelsCell modelCytotoxic effectsCells
2006
Illuminating the role of caspases during Drosophila oogenesis
Mazzalupo S, Cooley L. Illuminating the role of caspases during Drosophila oogenesis. Cell Death & Differentiation 2006, 13: 1950-1959. PMID: 16528381, DOI: 10.1038/sj.cdd.4401892.Peer-Reviewed Original ResearchConceptsNurse cell deathCaspase activityCell deathNurse cellsFluorescent proteinApoptosis protein 1Caspase inhibitor p35Caspase cleavage siteStarvation-induced deathRole of caspasesStarvation-induced apoptosisCyan fluorescent proteinYellow fluorescent proteinDrosophila inhibitorGermline developmentDrosophila oogenesisNormal oogenesisPoor environmental conditionsOogenesisCleavage siteProtein 1Environmental conditionsCaspasesProteinOocytes
2001
Normal Programmed Cell Death of Developing Avian and Mammalian Neurons Following Inhibition or Genetic Deletion of Caspases
Oppenheim R, Kuan C, Prevette D, Rakic P, Yaginuma H. Normal Programmed Cell Death of Developing Avian and Mammalian Neurons Following Inhibition or Genetic Deletion of Caspases. Research And Perspectives In Neurosciences 2001, 61-74. DOI: 10.1007/978-3-662-04333-2_6.Peer-Reviewed Original ResearchCell deathAbsence of caspasesProgrammed Cell DeathCaspase family membersPost-mitotic neuronsGenetic deletionCaspase inhibitorsCaspase activityNeuronal PCDMammalian neuronsPCDCaspasesChick embryosDeletionFamily membersMorphological degenerationEmbryosUpstreamNeuronsNormal occurrenceInhibitorsOvoInhibitionMembersDeath
2000
Mitochondrial and extramitochondrial apoptotic signaling pathways in cerebrocortical neurons
Budd S, Tenneti L, Lishnak T, Lipton S. Mitochondrial and extramitochondrial apoptotic signaling pathways in cerebrocortical neurons. Proceedings Of The National Academy Of Sciences Of The United States Of America 2000, 97: 6161-6166. PMID: 10811898, PMCID: PMC18575, DOI: 10.1073/pnas.100121097.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine TriphosphateAnimalsApoptosisBongkrekic AcidCaspase 3Caspase 8Caspase 9CaspasesCerebral CortexCytochrome c GroupEnzyme ActivationEnzyme InhibitorsIntracellular MembranesMitochondriaMitochondrial ADP, ATP TranslocasesNerve Tissue ProteinsNeuronsPermeabilityProtein Kinase InhibitorsReceptors, N-Methyl-D-AspartateStaurosporineConceptsAdenine nucleotide translocatorBongkrekic acidCaspase-3 activationMitochondrial adenine nucleotide translocatorCyt cReceptor-mediated apoptosisApoptotic signaling pathwaysMitochondrial permeability transition poreMitochondrial membrane potentialPermeability transition poreStaurosporine-induced activationCellular ATP contentStaurosporine resultsPutative componentsCerebrocortical neuronsNucleotide translocatorCaspase activityCaspase-8Signaling pathwaysTransition poreMitochondrial dysfunctionCytochrome cDistinct pathwaysCultured cerebrocortical neuronsApoptosis
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