2023
TMEM106B Puncta Is Increased in Multiple Sclerosis Plaques, and Reduced Protein in Mice Results in Delayed Lipid Clearance Following CNS Injury
Shafit-Zagardo B, Sidoli S, Goldman J, DuBois J, Corboy J, Strittmatter S, Guzik H, Edema U, Arackal A, Botbol Y, Merheb E, Nagra R, Graff S. TMEM106B Puncta Is Increased in Multiple Sclerosis Plaques, and Reduced Protein in Mice Results in Delayed Lipid Clearance Following CNS Injury. Cells 2023, 12: 1734. PMID: 37443768, PMCID: PMC10340176, DOI: 10.3390/cells12131734.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsEncephalomyelitis, Autoimmune, ExperimentalLipidsMiceMultiple SclerosisMyelin-Oligodendrocyte GlycoproteinSpinal CordConceptsAxonal damageMultiple sclerosisRelapsing-remitting multiple sclerosisHypomorphic miceExperimental autoimmune encephalomyelitisRelapsing-remitting MSNormal-appearing white matterMultiple sclerosis plaquesWhite matter plaquesNon-neurologic controlsWild-type miceBrains of individualsLipid droplet accumulationAutoimmune encephalomyelitisMyelin oligodendrocyteCNS injuryLipid clearanceSpinal cordNeuronal integrityTransmembrane protein 106BWhite matterAlzheimer's diseaseMice resultsDroplet accumulationPlaques
2012
Limiting multiple sclerosis related axonopathy by blocking Nogo receptor and CRMP-2 phosphorylation
Petratos S, Ozturk E, Azari MF, Kenny R, Lee JY, Magee KA, Harvey AR, McDonald C, Taghian K, Moussa L, Aui P, Siatskas C, Litwak S, Fehlings MG, Strittmatter SM, Bernard CC. Limiting multiple sclerosis related axonopathy by blocking Nogo receptor and CRMP-2 phosphorylation. Brain 2012, 135: 1794-1818. PMID: 22544872, PMCID: PMC3589918, DOI: 10.1093/brain/aws100.Peer-Reviewed Original ResearchMeSH KeywordsAdultAnalysis of VarianceAnimalsAntibodiesAxonsCD3 ComplexCell Line, TumorDemyelinating DiseasesDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalFemaleGene Expression RegulationGlycoproteinsGPI-Linked ProteinsGreen Fluorescent ProteinsHumansImmunoprecipitationIntercellular Signaling Peptides and ProteinsMaleMiceMice, Inbred C57BLMice, KnockoutMiddle AgedMultiple SclerosisMutationMyelin ProteinsMyelin-Oligodendrocyte GlycoproteinNerve DegenerationNerve Tissue ProteinsNeuroblastomaNeurofilament ProteinsNogo Receptor 1Optic NervePeptide FragmentsPhosphorylationReceptors, Cell SurfaceRetinal Ganglion CellsSeverity of Illness IndexSilver StainingSpinal CordTau ProteinsTime FactorsTransduction, GeneticTubulinConceptsExperimental autoimmune encephalomyelitisAutoimmune encephalomyelitisMyelin oligodendrocyte glycoproteinMultiple sclerosisAxonal degenerationSpinal cordChronic active multiple sclerosis lesionsOptic nerve axonal degenerationNogo-66 receptor 1CRMP-2Axonal growth inhibitorsCollapsin response mediator protein 2Improved clinical outcomesSpinal cord neuronsRetinal ganglion cellsResponse mediator protein 2Central nervous systemViable therapeutic targetAdeno-associated viral vectorMultiple sclerosis lesionsClinical outcomesOptic nerveCord neuronsOligodendrocyte glycoproteinGanglion cells
2010
MAG and OMgp Synergize with Nogo-A to Restrict Axonal Growth and Neurological Recovery after Spinal Cord Trauma
Cafferty WB, Duffy P, Huebner E, Strittmatter SM. MAG and OMgp Synergize with Nogo-A to Restrict Axonal Growth and Neurological Recovery after Spinal Cord Trauma. Journal Of Neuroscience 2010, 30: 6825-6837. PMID: 20484625, PMCID: PMC2883258, DOI: 10.1523/jneurosci.6239-09.2010.Peer-Reviewed Original ResearchMeSH KeywordsAnalysis of VarianceAnimalsBiotinCells, CulturedDextransDisease Models, AnimalFemaleFunctional LateralityGanglia, SpinalGPI-Linked ProteinsMaleMiceMice, Inbred C57BLMice, KnockoutMutationMyelin ProteinsMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinNerve Tissue ProteinsNeuronsNogo ProteinsPyramidal TractsReceptors, Cell SurfaceReceptors, SerotoninRecovery of FunctionSpinal Cord InjuriesConceptsAxonal growthSpinal Cord Injury StudyMutant miceGreater axonal growthGreater behavioral recoverySpinal cord traumaWild-type miceAxonal growth inhibitionHeterozygous mutant miceDeficient myelinNeurological recoveryCNS damageTriple-mutant miceBehavioral recoveryCord traumaFunctional recoveryNeurological functionMyelin inhibitorsAxonal regrowthReceptor mechanismsInjury studiesMyelin inhibitionDecoy receptorOptimal chanceMice
2004
Regulating axon growth within the postnatal central nervous system
Hu F, Strittmatter SM. Regulating axon growth within the postnatal central nervous system. Seminars In Perinatology 2004, 28: 371-378. PMID: 15693393, DOI: 10.1053/j.semperi.2004.10.001.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonsCentral Nervous SystemGPI-Linked ProteinsGrowth InhibitorsHumansHypoxiaIntracellular Signaling Peptides and ProteinsMembrane ProteinsMiceMyelin ProteinsMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinNerve RegenerationNerve Tissue ProteinsNogo ProteinsNogo Receptor 1Receptor, Nerve Growth FactorReceptors, Cell SurfaceConceptsCentral nervous systemAxonal growthNervous systemNeuronal developmentAdult central nervous systemMature central nervous systemAxon growth inhibitorsPostnatal central nervous systemPotential therapeutic interventionsNew neuronal connectionsMyelin-derived proteinsAxonal sproutingDirect blockadeNgR proteinPostnatal brainNeuronal connectionsTherapeutic interventionsAxon growthDevelopmental hypoxiaReduced expressionMyelin proteinsHypoxic conditionsInhibitor pathwayImportant investigationCritical roleBlockade of Nogo-66, Myelin-Associated Glycoprotein, and Oligodendrocyte Myelin Glycoprotein by Soluble Nogo-66 Receptor Promotes Axonal Sprouting and Recovery after Spinal Injury
Li S, Liu BP, Budel S, Li M, Ji B, Walus L, Li W, Jirik A, Rabacchi S, Choi E, Worley D, Sah DW, Pepinsky B, Lee D, Relton J, Strittmatter SM. Blockade of Nogo-66, Myelin-Associated Glycoprotein, and Oligodendrocyte Myelin Glycoprotein by Soluble Nogo-66 Receptor Promotes Axonal Sprouting and Recovery after Spinal Injury. Journal Of Neuroscience 2004, 24: 10511-10520. PMID: 15548666, PMCID: PMC6730300, DOI: 10.1523/jneurosci.2828-04.2004.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonsEvoked Potentials, MotorFemaleGPI-Linked ProteinsInjections, SpinalMotor ActivityMyelin ProteinsMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinNogo ProteinsNogo Receptor 1OligodendrogliaPeptide FragmentsRatsRats, Sprague-DawleyReceptors, Cell SurfaceReceptors, PeptideRecombinant Fusion ProteinsSerotoninSolubilitySpinal CordSpinal Cord InjuriesConceptsAxonal sproutingTraumatic spinal cord injurySpinal-injured ratsSpinal cord injuryAdult mammalian CNSNogo-66 receptorOligodendrocyte myelin glycoproteinMyelin associated glycoproteinRaphespinal fibersLocomotor recoveryCord injurySpinal injuryMammalian CNSNgR functionTherapeutic potentialAxonal growthNogo-66Myelin glycoproteinInjuryMyelin proteinsImproved locomotionViral blockadeBlockadeFc proteinSprouting
2003
The Nogo-66 receptor: focusing myelin inhibition of axon regeneration
McGee AW, Strittmatter SM. The Nogo-66 receptor: focusing myelin inhibition of axon regeneration. Trends In Neurosciences 2003, 26: 193-198. PMID: 12689770, DOI: 10.1016/s0166-2236(03)00062-6.Peer-Reviewed Original ResearchMeSH KeywordsAcute-Phase ProteinsAnimalsAxonsCells, CulturedGPI-Linked ProteinsHumansIn Vitro TechniquesMiceMyelin ProteinsMyelin SheathMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinNerve RegenerationNeural InhibitionNeuronal PlasticityNogo ProteinsNogo Receptor 1RatsReceptor, Nerve Growth FactorReceptors, Cell SurfaceReceptors, Nerve Growth FactorSignal TransductionConceptsNogo-66 receptorMembrane protein NogoSpinal cord injuryFunctional recoveryCord injuryAxonal regrowthSecond messenger pathwaysProtein NogoAdult CNSAxon regenerationMyelin inhibitionAxonal outgrowthAdditional studiesCNS myelinMyelinNeurite elongationPhysiological roleReceptorsMolecular determinantsInhibitorsInhibitionNGRCurrent understanding