2022
Characterization of temporospatial distribution of renal tubular casts by nephron tracking after ischemia-reperfusion injury
Shin NS, Marlier A, Xu L, Lam T, Cantley LG, Guo JK. Characterization of temporospatial distribution of renal tubular casts by nephron tracking after ischemia-reperfusion injury. American Journal Of Physiology. Renal Physiology 2022, 322: f322-f334. PMID: 35100823, PMCID: PMC8897010, DOI: 10.1152/ajprenal.00284.2021.Peer-Reviewed Original ResearchConceptsIschemia-reperfusion injuryCast formationGlomerular filtration rateTubular cast formationUrine 24 hDetached epithelial cellsDead cell debrisRenal recoveryRenal functionFiltration rateS3 tubulesTubular castsTubular cellsTubular nucleiKidney sectionsOuter medullaTrypsin levelsEntire nephronRenal tubular castsFuture interventionsInjurySelective lossTubule segmentsEpithelial cellsKidney
2021
Disordered breathing in a Pitt-Hopkins syndrome model involves Phox2b-expressing parafacial neurons and aberrant Nav1.8 expression
Cleary C, James S, Maher B, Mulkey D. Disordered breathing in a Pitt-Hopkins syndrome model involves Phox2b-expressing parafacial neurons and aberrant Nav1.8 expression. Nature Communications 2021, 12: 5962. PMID: 34645823, PMCID: PMC8514575, DOI: 10.1038/s41467-021-26263-2.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBasic Helix-Loop-Helix Transcription FactorsBenzimidazolesBrain StemCarbon DioxideDisease Models, AnimalFaciesGene Expression RegulationHaploinsufficiencyHomeodomain ProteinsHumansHyperventilationIntellectual DisabilityMaleMiceMice, KnockoutNAV1.8 Voltage-Gated Sodium ChannelNeuronsPsychomotor PerformancePyrazolesRespirationTranscription Factor 4Transcription FactorsConceptsPitt-Hopkins syndromeParafacial neuronsBreathing problemsEpisodes of hyperventilationFunction of neuronsNav1.8 expressionPTH patientsRetrotrapezoid nucleusNav1.8 channelsTranscription factor 4Behavioral deficitsMouse modelRespiratory functionBehavioral abnormalitiesTherapeutic potentialSyndrome modelDevelopmental delaySelective lossNeuronsIntellectual disabilityFactor 4Functional haploinsufficiencyBehavioral levelNav1.8ApneaChromatin remodeler Arid1a regulates subplate neuron identity and wiring of cortical connectivity
Doyle D, Lam M, Qalieh A, Qalieh Y, Sorel A, Funk O, Kwan K. Chromatin remodeler Arid1a regulates subplate neuron identity and wiring of cortical connectivity. Proceedings Of The National Academy Of Sciences Of The United States Of America 2021, 118: e2100686118. PMID: 34011608, PMCID: PMC8166177, DOI: 10.1073/pnas.2100686118.Peer-Reviewed Original ResearchMeSH KeywordsAbnormalities, MultipleAnimalsCerebral CortexChromatinConnectomeCorpus CallosumDNA-Binding ProteinsFaceGene DeletionGene Expression RegulationGray MatterHand Deformities, CongenitalHumansIntellectual DisabilityLoss of Function MutationMiceMice, TransgenicMicrognathismNeckNeural PathwaysNeuronsThalamusTranscription FactorsVibrissaeWhite MatterConceptsSubplate neuronsCorpus callosumThalamocortical Axon TargetingNeural circuit wiringCoffin-Siris syndromeSubplate ablationThalamocortical neuronsCallosal axonsAscending axonsBarrel developmentIntracortical axonsCortical developmentCortical connectivityWhite matterAxon targetingWhisker barrelsSelective lossNeuron identityExtracellular matrixAxonsCircuit wiringFunction mutationsCallosumAxon guidanceDevelopmental disorders
2020
KTN1 Variants Underlying Putamen Gray Matter Volumes and Parkinson’s Disease
Mao Q, Wang X, Chen B, Fan L, Wang S, Zhang Y, Lin X, Cao Y, Wu YC, Ji J, Xu J, Zheng J, Zhang H, Zheng C, Chen W, Cheng W, Luo X, Wang K, Zuo L, Kang L, Li CR, Luo X. KTN1 Variants Underlying Putamen Gray Matter Volumes and Parkinson’s Disease. Frontiers In Neuroscience 2020, 14: 651. PMID: 32655362, PMCID: PMC7324786, DOI: 10.3389/fnins.2020.00651.Peer-Reviewed Original ResearchPutamen gray matter volumesSubstantia nigra pars compactaGray matter volumeParkinson's diseaseMRNA expressionSingle nucleotide polymorphismsPD riskIndependent cohortMatter volumeDevelopment of PDPars compactaDopaminergic neuronsPutamenPutamen volumeSignificant associationPD associationsRisk allelesDiseaseSelective lossCohortGene variants
2012
Integrin β1 Signals through Arg to Regulate Postnatal Dendritic Arborization, Synapse Density, and Behavior
Warren MS, Bradley WD, Gourley SL, Lin YC, Simpson MA, Reichardt LF, Greer CA, Taylor JR, Koleske AJ. Integrin β1 Signals through Arg to Regulate Postnatal Dendritic Arborization, Synapse Density, and Behavior. Journal Of Neuroscience 2012, 32: 2824-2834. PMID: 22357865, PMCID: PMC3313657, DOI: 10.1523/jneurosci.3942-11.2012.Peer-Reviewed Original ResearchMeSH Keywordsalpha-FetoproteinsAnalysis of VarianceAnimalsAnimals, NewbornAvoidance LearningBasic Helix-Loop-Helix Transcription FactorsCells, CulturedCocaineDendritesEnzyme-Linked Immunosorbent AssayExploratory BehaviorGreen Fluorescent ProteinsGTPase-Activating ProteinsHippocampusImmunoprecipitationIntegrin beta1MaleMiceMice, KnockoutMutationNerve Tissue ProteinsNeuronsOrgan Culture TechniquesPost-Synaptic DensityProtein BindingRecognition, PsychologyRepressor ProteinsSignal Transductionsrc Homology DomainsSynapsesConceptsIntegrin β1Vertebrate nervous systemExtracellular matrix receptorsGenetic experimentsIntracellular tailGenetic manipulationRhoA GTPaseArg kinaseMatrix receptorsProper hippocampal functionProper developmentSynapse maintenanceDose-sensitive mannerImpaired hippocampus-dependent learningHippocampal dendritic arborsHippocampal synapse lossDendritic arbor sizeHippocampus-dependent learningΒ1ArgSelective lossGTPaseP190RhoGAPPsychomotor sensitivityKinase
2008
ICOS-dependent extrafollicular helper T cells elicit IgG production via IL-21 in systemic autoimmunity
Odegard JM, Marks BR, DiPlacido LD, Poholek AC, Kono DH, Dong C, Flavell RA, Craft J. ICOS-dependent extrafollicular helper T cells elicit IgG production via IL-21 in systemic autoimmunity. Journal Of Experimental Medicine 2008, 205: 2873-2886. PMID: 18981236, PMCID: PMC2585848, DOI: 10.1084/jem.20080840.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, CDAntigens, Differentiation, T-LymphocyteAutoimmunityCell DifferentiationChemokinesDisease Models, AnimalGerminal CenterImmunoglobulin Class SwitchingImmunoglobulin GInducible T-Cell Co-Stimulator ProteinInterleukinsLupus Erythematosus, SystemicMembrane GlycoproteinsMiceMice, KnockoutPlasma CellsReceptors, CXCR4T-Lymphocyte SubsetsT-Lymphocytes, Helper-InducerConceptsEffector T cellsT cellsIL-21IgG productionCXC chemokine receptor 4 (CXCR4) expressionB cell helper functionFollicular helper T cellsChemokine receptor 4 expressionReceptor 4 expressionCD4 T cellsHelper T cellsMRL/MpJAutoimmune strainsP-selectin glycoprotein ligand-1Autoantibody productionChronic autoimmunitySystemic autoimmunityPlasma cellsExtrafollicular responseExtrafollicular sitesMouse modelGerminal centersHelper functionSelective lossLigand 1
2007
A comparative study of proteasomal inhibition and apoptosis induced in N27 mesencephalic cells by dopamine and MG132
Zafar K, Inayat‐Hussain S, Ross D. A comparative study of proteasomal inhibition and apoptosis induced in N27 mesencephalic cells by dopamine and MG132. Journal Of Neurochemistry 2007, 102: 913-921. PMID: 17504267, DOI: 10.1111/j.1471-4159.2007.04637.x.Peer-Reviewed Original ResearchMeSH KeywordsAcetylcysteineAnimalsApoptosisCaspasesCell Line, TransformedCysteine Proteinase InhibitorsDopamineDose-Response Relationship, DrugEnzyme ActivationLeupeptinsMesencephalonNerve DegenerationNeuronsOxidative StressParkinson DiseaseProteasome Endopeptidase ComplexRatsReactive Oxygen SpeciesSubstantia NigraConceptsN-acetylcysteineN27 cellsParkinson's diseaseProteasomal inhibitionAbility of dopamineCell deathCaspase-9Dopaminergic neuronsDopaminergic cellsMesencephalic cellsDA treatmentConcentration-dependent apoptosisMG132-induced apoptosisCaspase-dependent apoptosisDiseaseSelective lossMitochondrial membrane potential lossReactive oxygen speciesDopamineCaspase-3Membrane potential lossApoptosisInhibitionQuinoid metabolitesCaspase-2
2001
Increased filamin binding to β-integrin cytoplasmic domains inhibits cell migration
Calderwood D, Huttenlocher A, Kiosses W, Rose D, Woodside D, Schwartz M, Ginsberg M. Increased filamin binding to β-integrin cytoplasmic domains inhibits cell migration. Nature Cell Biology 2001, 3: 1060-1068. PMID: 11781567, DOI: 10.1038/ncb1201-1060.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SubstitutionAnimalsBinding SitesCell MovementCell PolarityCHO CellsContractile ProteinsCricetinaeCytoplasmCytoskeletonFibronectinsFilaminsFocal AdhesionsHumansIntegrin beta ChainsIntegrinsIsoleucineJurkat CellsMicrofilament ProteinsProtein Structure, TertiaryRecombinant Fusion ProteinsTalinValineConceptsFocal adhesion formationFilamin bindingCell migrationMembrane protrusionsMatrix assemblyIntegrin-dependent cell migrationFibronectin matrix assemblyAmino acid substitutionsInhibits cell migrationAnimal developmentActin cytoskeletonIntegrin tailsBiochemical signalsAdhesion receptorsFilaminCell polarizationTalinAcid substitutionsExtracellular matrixAdhesion formationTailBindingAssemblyMigrationSelective loss
1997
Relationship between the Ocular Dominance and Orientation Maps in Visual Cortex of Monocularly Deprived Cats
Crair M, Ruthazer E, Gillespie D, Stryker M. Relationship between the Ocular Dominance and Orientation Maps in Visual Cortex of Monocularly Deprived Cats. Neuron 1997, 19: 307-318. PMID: 9292721, DOI: 10.1016/s0896-6273(00)80941-1.Peer-Reviewed Original ResearchConceptsCortical plasticityVisual cortexSame stimulus orientationSingle-unit recordingsStimulus orientationDeprived eyeIntrinsic optical signalsMonocular deprivationOcular dominanceOcular dominance mapsSelective lossOrientation tuningClosed eyesCritical periodCortexEyesNeuronsFunctional mapsBrief periodCompelling evidenceKittens
1995
Selective loss of slow and enhancement of fast Na+currents in cutaneous afferent dorsal root ganglion neurones following axotomy
Rizzo M, Kocsis J, Waxman S. Selective loss of slow and enhancement of fast Na+currents in cutaneous afferent dorsal root ganglion neurones following axotomy. Neurobiology Of Disease 1995, 2: 87-96. PMID: 8980012, DOI: 10.1006/nbdi.1995.0009.Peer-Reviewed Original Research
1987
Spinal cord α2-adrenoceptors may be located postsynaptically with respect to primary sensory neurons: Destruction of primary C-afferents with neonatal capsaicin does not affect the number of [3H]clonidine binding sites in mice
Wikberg J, Hajós M. Spinal cord α2-adrenoceptors may be located postsynaptically with respect to primary sensory neurons: Destruction of primary C-afferents with neonatal capsaicin does not affect the number of [3H]clonidine binding sites in mice. Neuroscience Letters 1987, 76: 63-68. PMID: 3035432, DOI: 10.1016/0304-3940(87)90193-5.Peer-Reviewed Original ResearchConceptsPrimary sensory neuronsSpinal cordSensory neuronsFmol/Capsaicin-treated animalsAfferent C-fibersNeonatal capsaicinNociceptive transmissionC-afferentsPain sensitivityC-fibersControl animalsCapsaicinMarked reductionSelective lossSecond dayContent of alphaCordAlphaMiceNeuronsLarge proportionAnimalsClonidineAgonists
1983
Cyclic Nucleotide‐Dependent Protein Kinases and Some Major Substrates in the Rat Cerebellum After Neonatal X‐Irradiation
Dolphin A, Detre J, Schlichter D, Nairn A, Yeh H, Woodward D, Greengard P. Cyclic Nucleotide‐Dependent Protein Kinases and Some Major Substrates in the Rat Cerebellum After Neonatal X‐Irradiation. Journal Of Neurochemistry 1983, 40: 577-581. PMID: 6296321, DOI: 10.1111/j.1471-4159.1983.tb11321.x.Peer-Reviewed Original Research
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