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Journal of Neuroscience, Vol 10, 3576-3582, Copyright © 1990 by Society for Neuroscience
Inhibition of agrin-induced acetylcholine-receptor aggregation by heparin, heparan sulfate, and other polyanions
BG Wallace
Department of Neurobiology, Stanford University School of Medicine, California 94305.
Heparin and heparan sulfate have been shown to block nerve-induced
acetylcholine-receptor (AChR) aggregation at developing neuromuscular
junctions. We found that heparin, heparan sulfate, and a wide variety of
other polyanions also inhibited agrin-induced AChR aggregation. The more
highly charged the polyanion, the more potent it was as an inhibitor.
Inhibition of agrin-induced AChR aggregation was due, at least in part, to
the formation of a complex between the polyanion and agrin that was
inactive. These findings are consistent with the hypothesis that
nerve-induced aggregation of AChRs is mediated by the release of agrin, or
a closely related protein, from axon terminals and suggest that a
polyanion, such as a sulfated proteoglycan, may be involved in the
interaction of agrin with its receptor on the myotube surface.
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