Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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 R., (2018), International Journal of Molecular Sciences, 19, 1326 - 1326

Serological and experimental studies in different forms of myasthenia gravis

Vincent A. et al, (2018), Annals of the New York Academy of Sciences, 1413, 143 - 153

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

Saxena A. et al, (2017), Scientific Reports, 7

Multiple roles of integrin-α3 at the neuromuscular junction

Ross JA. et al, (2017), Journal of Cell Science, 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), Experimental Neurology, 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), Human Molecular Genetics, 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 & Psychiatry, 83, A23.1 - A23

Presence and Pathogenic Relevance of Antibodies to Clustered Acetylcholine Receptor in Ocular and Generalized Myasthenia Gravis

Jacob S. et al, (2012), Archives of Neurology, 69

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), Experimental Neurology, 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

P23 Fluorescent receptors to light up the neuromuscular junction

Cossins J. et al, (2011), Neuromuscular Disorders, 21, S12 - S13

P33 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

Load More

Include forthcoming?