ArticleMuscle & nerve2009
Acetylcholine receptor-alpha subunit expression in myasthenia gravis: a role for the autoantigen in pathogenesis?
Article in Muscle & nerve, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Complement C3 inhibition restores myasthenia gravis AChR antibody-mediated muscle pathophysiology.EBioMedicine · 2026Article
- Decreased Serum 5-HT: Clinical Correlates and Regulatory Role in NMJ of MG.Annals of clinical and translational neurology · 2026Article
- Article
- Clinical significance of detection of antibodies to fetal and adult acetylcholine receptors in myasthenia gravis.Neuroscience bulletin · 2012Article
- Role of cytokines in the pathogenesis and suppression of thyroid autoimmunity.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2011Article
- B-cell-activating factor and autoimmune myasthenia gravis.Autoimmune diseases · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Previous studies have shown increased expression of acetylcholine receptor-alpha (AChR-alpha) subunit transcripts in myasthenia gravis (MG) and experimental MG (EAMG), but none examined the functional properties of this overexpression. In this study we examined the mRNA and protein expression of AChR-alpha as well as the pattern of alpha-bungarotoxin labeling in muscle tissue from EAMG mice with varying disease severity. AChR-alpha expression was increased considerably in endplates from mice with severe EAMG, but it was distinct and greatly in excess of alpha-bungarotoxin labeling. This "aberrant expression" occurred in mice with morphologic endplate damage, and the pattern of complement and immunoglobulin deposition in muscle from these mice appeared to mirror the pattern of AChR-alpha expression. The loss of functional AChR in severe MG increases transcription of AChR-alpha mRNA, but the expressed protein is "functionally inert," failing to compensate for loss of AChR. This enhanced expression of AChR may play a role in driving the ongoing autoimmune response. Muscle Nerve 40: 279-286, 2009.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.