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Publications

IgG1-3 MuSK Antibodies Inhibit AChR Cluster Formation, Restored by SHP2 Inhibitor, Despite Normal MuSK, DOK7, or AChR Subunit Phosphorylation.

Cao M. et al, (2023), Neurol Neuroimmunol Neuroinflamm, 10

NSC-87877, INHIBITOR OF SRC HOMOLOGY 2 DOMAIN-CONTAINING PHOSPHOTYROSINE PHOSPHATASE 2, AMELIORATES EXPERIMENTAL AUTOIMMUNE MYASTHENIA GRAVIS INDUCED BY MUSK IMMUNIZATION

Yilmaz V. et al, (2022), MUSCLE & NERVE, 65, S45 - S45

The Structure, Function, and Physiology of the Fetal and Adult Acetylcholine Receptor in Muscle.

Cetin H. et al, (2020), Front Mol Neurosci, 13

Interaction of Axonal Chondrolectin with Collagen XIXa1 Is Necessary for Precise Neuromuscular Junction Formation.

Oprişoreanu A-M. et al, (2019), Cell Rep, 29, 1082 - 1098.e10

Animal models of the neuromuscular junction, vitally informative for understanding function and the molecular mechanisms of congenital myasthenic syndromes

Webster RG., (2018), International Journal of Molecular Sciences, 19

Serological and experimental studies in different forms of myasthenia gravis.

Vincent A. et al, (2018), Ann N Y Acad Sci, 1413, 143 - 153

Characterization of an anti-fetal AChR monoclonal antibody isolated from a myasthenia gravis patient.

Saxena A. et al, (2017), Sci Rep, 7

Multiple roles of integrin-α3 at the neuromuscular junction.

Ross JA. et al, (2017), J Cell Sci, 130, 1772 - 1784

Fast-channel congenital myasthenic syndrome with a novel acetylcholine receptor mutation at the α-ε subunit interface

Webster R. et al, (2014), Neuromuscular Disorders, 24, 143 - 147

A mouse model of the slow channel myasthenic syndrome: Neuromuscular physiology and effects of ephedrine treatment.

Webster RG. et al, (2013), Exp Neurol, 248, 286 - 298

Mutations in GFPT1 that underlie limb-girdle congenital myasthenic syndrome result in reduced cell-surface expression of muscle AChR.

Zoltowska K. et al, (2013), Hum Mol Genet, 22, 2905 - 2913

Slow channel congenital myasthenic syndrome responsive to a combination of fluoxetine and salbutamol.

Finlayson S. et al, (2013), Muscle Nerve, 47, 279 - 282

FAST CHANNEL CONGENITAL MYASTHENIA: REVIEW OF 12 CASES AND TREATMENT CHALLENGES

Finlayson S. et al, (2012), JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY, 83, A23 - A23

Presence and pathogenic relevance of antibodies to clustered acetylcholine receptor in ocular and generalized myasthenia gravis.

Jacob S. et al, (2012), Arch Neurol, 69, 994 - 1001

A novel congenital myasthenic syndrome due to decreased acetylcholine receptor ion-channel conductance.

Webster R. et al, (2012), Brain, 135, 1070 - 1080

Passive and active immunization models of MuSK-Ab positive myasthenia: electrophysiological evidence for pre and postsynaptic defects.

Viegas S. et al, (2012), Exp Neurol, 234, 506 - 512

A novel congenital myasthenic syndrome due to decreased acetylcholine receptor ion-channel conductance

Webster R. et al, (2012), Brain, 135, 1070 - 1080

Fluorescent receptors to light up the neuromuscular junction

Cossins J. et al, (2011), NEUROMUSCULAR DISORDERS, 21, S12 - S13

Impaired neurotransmission in a mouse model of the slow channel congenital myasthenic syndrome is improved by the sympathomimetic drug ephedrine

Webster R. et al, (2011), NEUROMUSCULAR DISORDERS, 21, S15 - S15

Muscle dysfunction caused by a KATP channel mutation in neonatal diabetes is neuronal in origin.

Clark RH. et al, (2010), Science, 329, 458 - 461

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