ArticleThe Journal of clinical investigation1998
Regulation of acetylcholine receptor gene expression in human myasthenia gravis muscles. Evidences for a compensatory mechanism triggered by receptor loss.
Article in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 64 citations in OpenAlex.
- Complement C3 inhibition restores myasthenia gravis AChR antibody-mediated muscle pathophysiology.EBioMedicine · 2026Article
- Aging Does Not Exacerbate Muscle Loss During Denervation and Lends Unique Muscle-Specific Atrophy Resistance With Akt Activation.Frontiers in physiology · 2021Article
- The Muscle Is Not a Passive Target in Myasthenia Gravis.Frontiers in neurology · 2019Review
- Crossreactivity of an Antiserum Directed to the Gram-Negative Bacterium Neisseria gonorrhoeae with the SNARE-Complex Protein Snap23 Correlates to Impaired Exocytosis in SH-SY5Y Cells.Journal of molecular neuroscience : MN · 2017Article
- Neuromuscular junction degeneration in muscle wasting.Current opinion in clinical nutrition and metabolic care · 2016Review
- IL-6 and Akt are involved in muscular pathogenesis in myasthenia gravis.Acta neuropathologica communications · 2015Article
- Biomechanical strain vehicles for fibroblast-directed skeletal myoblast differentiation and myotube functionality in a novel coculture.American journal of physiology. Cell physiology · 2014Article
- Protective effect of scFv-DAF fusion protein on the complement attack to acetylcholine receptor: a possible option for treatment of myasthenia gravis.Muscle & nerve · 2012Article
- Mechanisms underlying autoimmune synaptic encephalitis leading to disorders of memory, behavior and cognition: insights from molecular, cellular and synaptic studies.The European journal of neuroscience · 2010Review
- Acetylcholine receptor-alpha subunit expression in myasthenia gravis: a role for the autoantigen in pathogenesis?Muscle & nerve · 2009Article
- Establishment of a human thymic myoid cell line. Phenotypic and functional characteristics.The American journal of pathology · 1999Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myasthenia gravis (MG) is a neuromuscular disorder mediated by antibodies directed against the acetylcholine receptor (nAChR) resulting in a functional nAChR loss. To analyze the molecular mechanisms involved at the muscular target site, we studied the expression of nAChR subunits in muscle biopsy specimens from MG patients. By using quantitative PCR with an internal standard for each subunit, we found that the levels of beta-, delta-, and epsilon-subunit mRNA coding for the adult nAChR were increased in severely affected MG patients, matching our previous data on the alpha-subunit. Messenger levels were highly variable in MG patients but not in controls, pointing to individual factors involved in the regulation of nAChR genes. The fetal subunit (gamma-chain) transcripts were almost undetectable in the extrajunctional region of MG muscle, suggesting that gene regulation in MG differs from that in the denervation model, in which nAChR gamma-subunit mRNA is reexpressed. Nicotinic AChR loss mediated by monoclonal anti-nAChR antibodies in both the TE671 muscle cell line and cultured normal human myotubes induces a similar increase in beta- alphand delta-subunit mRNA levels, suggesting the existence of a new muscular signaling pathway system coupled to nAChR internalization and independent of muscle electrical activity. These data demonstrate the existence of a compensatory mechanism regulating the expression of the genes coding for the adult nAChR in patients with MG.
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