2019
Loss of Protein Kinase Csnk2b/CK2β at Neuromuscular Junctions Affects Morphology and Dynamics of Aggregated Nicotinic Acetylcholine Receptors, Neuromuscular Transmission, and Synaptic Gene Expression
Eiber N, Rehman M, Kravic B, Rudolf R, Sandri M, Hashemolhosseini S. Loss of Protein Kinase Csnk2b/CK2β at Neuromuscular Junctions Affects Morphology and Dynamics of Aggregated Nicotinic Acetylcholine Receptors, Neuromuscular Transmission, and Synaptic Gene Expression. Cells 2019, 8: 940. PMID: 31434353, PMCID: PMC6721821, DOI: 10.3390/cells8080940.Peer-Reviewed Original ResearchConceptsSynaptic gene expressionGene expressionNicotinic acetylcholine receptorsClustering of AChRsNeuromuscular junctionCultured muscle cellsAcetylcholine receptorsDistinctive proteinsCK2Neuromuscular transmissionAChR clustersΒ-subunitCompound muscle action potentialHigh turnover rateCK2βCell proliferationMuscle action potentialsNMJ fragmentationSkeletal muscle fibersPrecise roleAge-dependent decreaseMuscle cellsAcetylcholine esterase inhibitorsAChRExpression
1996
Real-time detection of the surface delivery of newly synthesized membrane proteins.
Andreose JS, Fumagalli G, Sigworth FJ, Caplan MJ. Real-time detection of the surface delivery of newly synthesized membrane proteins. Proceedings Of The National Academy Of Sciences Of The United States Of America 1996, 93: 7661-7666. PMID: 8755532, PMCID: PMC38803, DOI: 10.1073/pnas.93.15.7661.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBungarotoxinsCell LineCell MembraneElectrophysiologyFourier AnalysisGolgi ApparatusGuanosine 5'-O-(3-Thiotriphosphate)Guanosine TriphosphateIon ChannelsKineticsMembrane PotentialsMembrane ProteinsMiceMuscle, SkeletalProtein Processing, Post-TranslationalReceptors, NicotinicTime FactorsConceptsMembrane proteinsPlasma membraneCell surfaceDegrees C temperature blockCultured muscle cellsConstitutive trafficTransport vesiclesConstitutive deliveryFusion eventsSurface deliveryFusion poreExocytotic vesiclesAChR moleculeGolgi complexTemperature blockAChR proteinNicotinic acetylcholine receptorsIon channel propertiesMost cellsVesiclesProteinCurrent fluctuationsMuscle cellsAcetylcholine receptorsGuanosine 5'The lethal hemolytic mutation in beta I sigma 2 spectrin Providence yields a null phenotype in neonatal skeletal muscle.
Weed SA, Stabach PR, Oyer CE, Gallagher PG, Morrow JS. The lethal hemolytic mutation in beta I sigma 2 spectrin Providence yields a null phenotype in neonatal skeletal muscle. Laboratory Investigation 1996, 74: 1117-29. PMID: 8667615.Peer-Reviewed Original ResearchConceptsBeta ISpectrin skeletonSkeletal muscleMost such mutationsGene transferAdult mouse skeletal muscleDominant-negative fashionErythroid lineage cellsNeonatal skeletal muscleCultured muscle cellsAlpha beta heterodimersErythrocyte shape abnormalitiesMuscle cellsMouse skeletal muscleDefective proteinSpectrin geneAlternative transcriptsHemolytic phenotypeCDNA constructsNull phenotypeC2C12 myoblastsBeta heterodimerSpectrin mutationsSedimentation velocity analysisIntracellular distribution
1983
The acetylcholine receptor as a cellular receptor for rabies virus.
Lentz T, Burrage T, Smith A, Tignor G. The acetylcholine receptor as a cellular receptor for rabies virus. The Yale Journal Of Biology And Medicine 1983, 56: 315-22. PMID: 6367238, PMCID: PMC2589619.Peer-Reviewed Original ResearchConceptsAcetylcholine receptorsHost cell receptorsRabies virusSpecific host cell receptorsCell receptorTissue tropismMotor nerve endingsRabies virus pathogenesisMyasthenia gravisAutoimmune diseasesCultured muscle cellsNerve endingsTranssynaptic transferViral antigensViral immunizationVirus pathogenesisDisease processNeurotransmitter receptorsViral infectionIntact hostCellular tropismNeuromuscular junctionInfected animalsMuscle cellsVirus attachment
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