| First Author | Mitsui T | Year | 1996 |
| Journal | Biochem Biophys Res Commun | Volume | 224 |
| Issue | 3 | Pages | 802-7 |
| PubMed ID | 8713126 | Mgi Jnum | J:34495 |
| Mgi Id | MGI:81951 | Doi | 10.1006/bbrc.1996.1103 |
| Citation | Mitsui T, et al. (1996) Induction of dystrophin-associated proteins together with nicotinic acetylcholine receptors by denervation in the absence of dystrophin in skeletal muscles of mdx mice. Biochem Biophys Res Commun 224(3):802-7 |
| abstractText | 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. |
