a point mutation on synaptotagmin located outside of the BoNT/B-binding segment inhibited GT1b binding and blocked GT1b-induced potentiation of BoNT/B binding to synaptotagmin-expressing cells.
Study showed postsynaptic localization of synaptotagmin 1 at concentrations moderately lower than but comparable to presynaptic concentrations. It is present in significant concentrations at the postsynaptic density pointing to the likelihood of insertion of glutamate receptors directly into the synaptic plasma membrane. Synaptotagmin 1 is reduced in postsynaptic spines after eight weeks of kainite-induced epilepsy.
Data suggest that GTP-binding protein beta/gamma (Gb/g) heterodimers interact specifically with lipid-embedded neuronal t-SNARE proteins syntaxin 1A and SNAP-25B (synaptosomal-associated protein 25B); this binding is competitive with synaptotagmin 1 for binding sites on the t-SNARE proteins; Gb/g inhibits Ca2+/synaptotagmin 1-dependent membrane fusion.
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