2025
α-Latrotoxin Actions in the Absence of Extracellular Ca2+ Require Release of Stored Ca2+
Blackburn J, Islam Q, Benlaouer O, Tonevitskaya S, Petitto E, Ushkaryov Y. α-Latrotoxin Actions in the Absence of Extracellular Ca2+ Require Release of Stored Ca2+. Toxins 2025, 17: 73. PMID: 39998090, PMCID: PMC11860464, DOI: 10.3390/toxins17020073.Peer-Reviewed Original ResearchConceptsAbsence of extracellular Ca<sup>2+</sup> anRelease of stored Ca2+Store-operated Ca<sup>2+</sup> entryExtracellular Ca<sup>2+</sup>Absence of extracellular Ca2Nerve terminalsCytosolic Ca<sup>2+</sup>Neurotransmitter releaseOpening of Ca<sup>2+</sup> channelsControl of neurotransmitter releaseRelease of neurotransmittersIntracellular storesExtracellular Ca2BAPTA-AMG protein-coupled receptorsMouse neuromuscular junctionCation ionophoreSensitive to inhibitorsCa2+Neuromuscular junctionNerveNeurotransmitterPhysiological controlReleaseInflux
2019
Characterization of pathogenic monoclonal autoantibodies derived from muscle-specific kinase myasthenia gravis patients
Takata K, Stathopoulos P, Cao M, Mané-Damas M, Fichtner ML, Benotti ES, Jacobson L, Waters P, Irani SR, Martinez-Martinez P, Beeson D, Losen M, Vincent A, Nowak RJ, O’Connor K. Characterization of pathogenic monoclonal autoantibodies derived from muscle-specific kinase myasthenia gravis patients. JCI Insight 2019, 4: e127167. PMID: 31217355, PMCID: PMC6629167, DOI: 10.1172/jci.insight.127167.Peer-Reviewed Original ResearchConceptsMyasthenia gravisMonoclonal autoantibodiesNeuromuscular junctionMuscle-specific tyrosine kinaseMuSK-MG patientsChronic autoimmune disorderMyasthenia gravis patientsSubset of patientsMouse neuromuscular junctionHuman monoclonal autoantibodiesMuSK autoantibodiesAutoimmune mechanismsGravis patientsMG patientsMost patientsPathogenic autoantibodiesAutoimmune disordersMuscle weaknessNeuromuscular transmissionMuSK phosphorylationAutoantibodiesB cellsAcetylcholine receptorsSynaptic differentiationPatients
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