The absence of dystrophin rather than XXXX causes acetylcholine receptor cluster defects in @entity121 .

@entity2383 @entity1949 @entity19 @entity1555 @entity842 @entity121 @entity934
@entity1555 is the most common genetic @entity121 . Affected muscles are characterized by abnormal @entity934 receptor (AChR) clustering. Some studies have suggested that changes in AChR clusters are secondary to degenerative processes. In this study, we demonstrate that AChR @entity1949 and @entity121 are separate events. We compared AChR clusters and pathological features in mdx @entity19 (mutated dystrophin) and dko @entity19 (mutated dystrophin and utrophin). AChR clusters were identified by binding with a-bungarotoxin, and pathological features were observed by classical immunohistochemical techniques. AChR clusters in mdx and dko @entity19 were reduced in number and exhibited @entity2383 . However, AChR @entity1949 was not significantly different in mdx and dko @entity19 , although more severe inflammatory infiltration and degeneration were observed in dko @entity19 . Furthermore, neuronal @entity842 synthase, which interacts with dystrophin to anchor itself at the sarcolemma, was notably reduced in mdx and dko @entity19 . Fragmentation of AChR and @entity121 are separate events, and both are secondary results of destabilization on the sarcolemma and the cytoskeleton.
