2006
Mitochondrial fission is an upstream and required event for bax foci formation in response to nitric oxide in cortical neurons
Yuan H, Gerencser A, Liot G, Lipton S, Ellisman M, Perkins G, Bossy-Wetzel E. Mitochondrial fission is an upstream and required event for bax foci formation in response to nitric oxide in cortical neurons. Cell Death & Differentiation 2006, 14: 462-471. PMID: 17053808, DOI: 10.1038/sj.cdd.4402046.Peer-Reviewed Original ResearchConceptsMitochondrial fissionNitric oxideFoci formationCortical neuronsMitochondrial fission machineryBcl-2 familyNitrosative stressAntiapoptotic Bcl-xLNeuronal cell deathFission machineryMitofusin 1Puncta formationBioenergetic crisisBax accumulationMitochondrial inhibitorsNeuronal demiseBcl-xLCell deathMitochondrial dysfunctionMitochondriaNeurodegenerative disordersNO donorNeuronsScission siteFission
2005
Nitrosative and oxidative stress links dysfunctional ubiquitination to Parkinson's disease
Gu Z, Nakamura T, Yao D, Shi Z, Lipton S. Nitrosative and oxidative stress links dysfunctional ubiquitination to Parkinson's disease. Cell Death & Differentiation 2005, 12: 1202-1204. PMID: 16094397, DOI: 10.1038/sj.cdd.4401705.Peer-Reviewed Original Research
1994
HIV-related neuronal injury
Lipton S. HIV-related neuronal injury. Molecular Neurobiology 1994, 8: 181-196. PMID: 7999315, DOI: 10.1007/bf02780669.Peer-Reviewed Original ResearchConceptsArachidonic acidExistence of HIVCalcium channel antagonistsVoltage-dependent Ca2Receptor-operated channelsFuture pharmacological interventionsFinal common pathwayAmyotrophic lateral sclerosisPlatelet-activating factorDysfunction of cognitionDemise of neuronsNeuropathic painAdult patientsAIDS dementiaNeuronal injuryNeurological manifestationsNeuronal damageImmunodeficiency syndromeAIDS patientsChannel antagonistsNMDA antagonistsNeuronal susceptibilityPharmacological interventionsLateral sclerosisParkinson's disease
1991
HIV‐Related Neurotoxicity
Lipton S. HIV‐Related Neurotoxicity. Brain Pathology 1991, 1: 193-199. PMID: 1669708, DOI: 10.1111/j.1750-3639.1991.tb00659.x.Peer-Reviewed Original ResearchConceptsNeuronal injuryCentral nervous system manifestationsL-type voltage-dependent calcium channelsVoltage-dependent calcium channelsNervous system manifestationsHIV-1 infectionToxic factorsWhite matter lesionsNeuronal cell deathIntracellular calcium concentrationNeuronal cell typesNeuronal lossSystem manifestationsMatter lesionsEndogenous glutamateImmune cellsGlutamate receptorsGp 120Human neuronsCalcium channelsGp120 fragmentRodent neuronsHIVGp120Potential neurotoxins