2012
N-terminally cleaved Bcl-xL mediates ischemia-induced neuronal death
Ofengeim D, Chen YB, Miyawaki T, Li H, Sacchetti S, Flannery RJ, Alavian KN, Pontarelli F, Roelofs BA, Hickman JA, Hardwick JM, Zukin RS, Jonas EA. N-terminally cleaved Bcl-xL mediates ischemia-induced neuronal death. Nature Neuroscience 2012, 15: 574-580. PMID: 22366758, PMCID: PMC3862259, DOI: 10.1038/nn.3054.Peer-Reviewed Original Research
2011
Bcl-xL regulates mitochondrial energetics by stabilizing the inner membrane potential
Chen YB, Aon MA, Hsu YT, Soane L, Teng X, McCaffery JM, Cheng WC, Qi B, Li H, Alavian KN, Dayhoff-Brannigan M, Zou S, Pineda FJ, O'Rourke B, Ko YH, Pedersen PL, Kaczmarek LK, Jonas EA, Hardwick JM. Bcl-xL regulates mitochondrial energetics by stabilizing the inner membrane potential. Journal Of Cell Biology 2011, 195: 263-276. PMID: 21987637, PMCID: PMC3198165, DOI: 10.1083/jcb.201108059.Peer-Reviewed Original ResearchConceptsMitochondrial membrane potentialMitochondrial membraneMitochondrial ATP synthase β-subunitATP synthase β subunitBcl-2 family proteinsOuter membrane permeabilizationInner mitochondrial membrane potentialMembrane potentialMitochondrial energetic capacityOuter mitochondrial membraneSynthase β subunitInner mitochondrial membraneInner membrane potentialATP synthaseFamily proteinsBiochemical approachesGenetic evidenceEndogenous BclMembrane permeabilizationCellular resourcesΒ-subunitBcl-xLMitochondrial energeticsEnergetic capacityMitochondrial cristae
2009
Elevated P75NTR expression causes death of engrailed-deficient midbrain dopaminergic neurons by Erk1/2 suppression
Alavian KN, Sgadò P, Alberi L, Subramaniam S, Simon HH. Elevated P75NTR expression causes death of engrailed-deficient midbrain dopaminergic neurons by Erk1/2 suppression. Neural Development 2009, 4: 11. PMID: 19291307, PMCID: PMC2667502, DOI: 10.1186/1749-8104-4-11.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlotting, WesternCell DeathCells, CulturedDisease Models, AnimalDopamineHeterozygoteHomeodomain ProteinsImmunohistochemistryMesencephalonMiceMice, Inbred C57BLMice, KnockoutMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3MutationNerve Tissue ProteinsNeuronsParkinson DiseaseReceptors, Nerve Growth FactorReverse Transcriptase Polymerase Chain ReactionUp-RegulationConceptsMesDA neuronsBcl-2 familyAnti-apoptotic membersCell death signalsExpression levelsMutant embryosHaplotype variationDeath signalsMitochondrial stabilityEngrailedERK1/2 activityEngrailed-1Mitochondrial insultDopaminergic neuronsGenesPostnatal maintenanceReceptor geneElevated expressionMidbrain dopaminergic neuronsHeterozygote animalsDependent mannerMutant miceNigrostriatal dopaminergic systemERK1/2 suppressionMesencephalic dopaminergic neurons
2006
Slow progressive degeneration of nigral dopaminergic neurons in postnatal Engrailed mutant mice
Sgadò P, Albéri L, Gherbassi D, Galasso SL, Ramakers GM, Alavian KN, Smidt MP, Dyck RH, Simon HH. Slow progressive degeneration of nigral dopaminergic neurons in postnatal Engrailed mutant mice. Proceedings Of The National Academy Of Sciences Of The United States Of America 2006, 103: 15242-15247. PMID: 17015829, PMCID: PMC1622807, DOI: 10.1073/pnas.0602116103.Peer-Reviewed Original ResearchConceptsDopaminergic neuronsProgressive degenerationParkinson's diseaseMutant miceEngrailed-1Postnatal mutant miceSlow progressive degenerationNigral dopaminergic neuronsMesencephalic dopaminergic neuronsRelease of dopamineKey pathological featureLower body weightMotor deficitsPathological featuresSubstantia nigraCaudate putamenNovel treatmentsBody weightNeurodegenerative disordersHeterozygous nullDiseaseMiceNeuronsMolecular etiologyDependent manner