Acetylcholine receptor turnover in mice with passively transferred myasthenia gravis. I. Receptor degradation.

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Acetylcholine receptor turnover in mice with passively transferred myasthenia gravis. I. Receptor degradation.

The in vivo degradation of endplate acetylcholine receptors was investigated in mice treated daily with IgG from 10 myasthenia gravis patients. Four preparations increased the rate of degradation. The number of endplate acetylcholine receptors after 7 days of IgG treatment was greater than that predicted on the basis of the increased degradation rate, suggesting a compensatory increase in recep...

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Acetylcholine receptor turnover in mice with passively transferred myasthenia gravis. II. Receptor synthesis.

The in vivo synthesis of diaphragm endplate acetylcholine receptors was estimated in mice treated daily with IgG from eight myasthenia gravis patients. Myasthenia gravis IgG preparations which had previously been shown to increase the rate of receptor degradation also increased the rate of receptor synthesis, suggesting the existence of a compensatory mechanism serving to stabilise the number o...

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Degradation of acetylcholine receptor in diaphragms of rats with experimental autoimmune myasthenia gravis.

The degradation of acetylcholine receptor observed in denervated and innervated normal rat diaphragms in organ culture is stimulated by exogenous antireceptor serum. In this paper we demonstrate that diaphragms from rats with experimental autoimmune myasthenia gravis contain reduced amounts of acetylcholine receptor. Acetylcholine receptor from myasthenic, but not from normal, rats has antibody...

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Deficiencies in anti-acetylcholine receptor antibody measurement in myasthenia gravis.

In a retrospective case note study of 86 patients with myasthenia gravis, 60 had an anti-acetylcholine receptor antibody assay performed by the regional immunology laboratory. Antibody was detected in 38% which compares with 66-93% in other series. Whilst the use of staphylococcal protein A to precipitate the antibody-receptor complex, rather than anti-human immunoglobulin, may be partly respon...

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Mechanisms of acetylcholine receptor loss in myasthenia gravis.

The fundamental abnormality affecting the neuromuscular junctions of myasthenic patients is a reduction of available AChRs, due to an autoimmune attack directed against the receptors. Antibodies to AChR are present in most patients, and there is evidence that they have a predominant pathogenic role in the disease, aided by complement. The mechanism of antibody action involves acceleration of th...

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ژورنال

عنوان ژورنال: Journal of Neurology, Neurosurgery & Psychiatry

سال: 1983

ISSN: 0022-3050

DOI: 10.1136/jnnp.46.5.377