Chemical Modification of Taipoxin and the Consequences for Phospholipase Activity, Pathophysiology, and Inhibition of High‐Affinity Choline Uptake

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Abstract
Treatment of taipoxin with p‐bromophenacyl bromide resulted in modification of single histidine residues in the α and β subunits. The modification decreased the neurotoxicity (lethality) 350‐fold, but the inhibitory action on high‐affinity choline transport was reduced only threefold. The phospholipase activity and Ca2+‐association constants for taipoxin and its subunits were determined. A model for the neurotoxicity of taipoxin indicates the α subunit as the ultimate cause of the disruption of synaptic transmission.

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