2022
Targeting RTN4/NoGo-Receptor reduces levels of ALS protein ataxin-2
Rodriguez CM, Bechek SC, Jones GL, Nakayama L, Akiyama T, Kim G, Solow-Cordero DE, Strittmatter SM, Gitler AD. Targeting RTN4/NoGo-Receptor reduces levels of ALS protein ataxin-2. Cell Reports 2022, 41: 111505. PMID: 36288715, PMCID: PMC9664481, DOI: 10.1016/j.celrep.2022.111505.Peer-Reviewed Original ResearchConceptsAmyotrophic lateral sclerosisSpinocerebellar ataxia type 2Nogo receptorAtaxin-2 levelsNovel therapeutic targetNeurodegenerative disease amyotrophic lateral sclerosisGene-based therapeutic strategiesDisease amyotrophic lateral sclerosisNerve injuryAtaxin-2Axonal regenerationAxonal regrowthLateral sclerosisTherapeutic strategiesHuman neuronsKnockout miceTherapeutic targetPotential treatmentType 2Protein levelsPotent modifierProtein ataxin-2Additional strategiesMiceRNA screen
2005
Nogo-A Interacts with the Nogo-66 Receptor through Multiple Sites to Create an Isoform-Selective Subnanomolar Agonist
Hu F, Liu BP, Budel S, Liao J, Chin J, Fournier A, Strittmatter SM. Nogo-A Interacts with the Nogo-66 Receptor through Multiple Sites to Create an Isoform-Selective Subnanomolar Agonist. Journal Of Neuroscience 2005, 25: 5298-5304. PMID: 15930377, PMCID: PMC2855126, DOI: 10.1523/jneurosci.5235-04.2005.Peer-Reviewed Original ResearchMeSH KeywordsAlkaline PhosphataseAnimalsAxonsBinding SitesCell LineChick EmbryoChlorocebus aethiopsGlutathione TransferaseGPI-Linked ProteinsHumansIn Vitro TechniquesLigandsMiceMyelin ProteinsNogo ProteinsNogo Receptor 1PeptidesProtein IsoformsProtein Structure, TertiaryReceptors, Cell SurfaceRecombinant Fusion Proteins
1997
A novel action of collapsin: Collapsin‐1 increases antero‐ and retrograde axoplasmic transport independently of growth cone collapse
Goshima Y, Kawakami T, Hori H, Sugiyama Y, Takasawa S, Hashimoto Y, Kagoshima‐Maezono M, Takenaka T, Misu Y, Strittmatter S. A novel action of collapsin: Collapsin‐1 increases antero‐ and retrograde axoplasmic transport independently of growth cone collapse. Developmental Neurobiology 1997, 33: 316-328. PMID: 9298768, DOI: 10.1002/(sici)1097-4695(199709)33:3<316::aid-neu9>3.0.co;2-4.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonal TransportCells, CulturedDose-Response Relationship, DrugGanglia, SpinalGlycoproteinsGTP-Binding ProteinsIntercellular Signaling Peptides and ProteinsMiceMice, Inbred C57BLMyelin ProteinsNerve Growth FactorsNeuritesOrganellesPeptidesPertussis ToxinSemaphorin-3AVirulence Factors, BordetellaWasp Venoms
1994
Activated mutants of the alpha subunit of G(o) promote an increased number of neurites per cell
Strittmatter S, Fishman M, Zhu X. Activated mutants of the alpha subunit of G(o) promote an increased number of neurites per cell. Journal Of Neuroscience 1994, 14: 2327-2338. PMID: 8158271, PMCID: PMC6577129, DOI: 10.1523/jneurosci.14-04-02327.1994.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsBase SequenceCell LineChlorocebus aethiopsDNA PrimersDose-Response Relationship, DrugGTP-Binding ProteinsIntercellular Signaling Peptides and ProteinsKineticsMacromolecular SubstancesMolecular Sequence DataMutagenesis, Site-DirectedNeuritesNeuroblastomaPC12 CellsPeptidesPertussis ToxinPoint MutationTransfectionTumor Cells, CulturedVirulence Factors, BordetellaWasp VenomsConceptsAlpha oNumber of neuritesPertussis toxin-sensitive G proteinToxin-sensitive G proteinGrowth conesAlpha subunitG proteinsNeurite outgrowthTotal neurite lengthN1E-115 cellsAlpha i2Activated alpha subunitNeuroblastoma cellsNeurite numberNeurite lengthNeuronal growth conesAlpha sOncogenic mutationsActivation stateO mutantsActivationNeuritesCellsPoint mutationsSubunits
1993
Mediation by G Proteins of Signals That Cause Collapse of Growth Cones
Igarashi M, Strittmatter S, Vartanian T, Fishman M. Mediation by G Proteins of Signals That Cause Collapse of Growth Cones. Science 1993, 259: 77-79. PMID: 8418498, DOI: 10.1126/science.8418498.Peer-Reviewed Original Research