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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Induction of dystrophin-associated proteins together with nicotinic acetylcholine receptors by denervation in the absence of dystrophin in skeletal muscles of mdx mice.

We purified the nicotinic acetylcholine receptor from digitonin-solubilized rabbit skeletal muscle by affinity chromatography and detected many proteins linked to AChR, including dystrophin, adhalin, beta-dystroglycan, utrophin, rapsyn, and actin. To determine whether or not AChR links to dystrophin-associated proteins (DAPs) without dystrophin, we studied the effects of denervation on AChR and DAPs in the skeletal muscle of a mdx mouse. Following surgical denervation, the levels of adhalin and beta-dystroglycan dramatically increased at the extrajunctional sarcolemma with AChR, suggesting that their association is independent of dystrophin. Furthermore, the diffuse extrajunctional appearance of adhalin, beta-dystroglycan, and AChR was observed after pharmacological denervation through the subcutaneous administration of succinylcholine. Since the depletion of DAPs and the subsequent disruption of sarcolemmal linkage are believed to be a primary cause of muscle cell necrosis in dystrophinopathies, pharmacological denervation may have some beneficial effect on these diseases.[1]

References

  1. Induction of dystrophin-associated proteins together with nicotinic acetylcholine receptors by denervation in the absence of dystrophin in skeletal muscles of mdx mice. Mitsui, T., Kawai, H., Kawajiri, M., Kunishige, M., Aki, K., Saito, S. Biochem. Biophys. Res. Commun. (1996) [Pubmed]
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