By analogy to the process described for botulinum toxin type A (Koriazova and Montal 2003; Montal 2010), acidification, a normal step in synaptic vesicle recycling, is inferred to cause a conformational change in the botulinum toxin type B disulfide bonded heavy chain - light chain dimer (botB HC:LC) it contains, allowing the HC part of the toxin to function as a channel through which its LC part is extruded into the neuronal cytosol. The HC - LC disulfide bond is cleaved. Recent studies in vitro suggest that GT1b ganglioside associated with the toxin may play a role in this process (Sun et al. 2011, 2012).
Tepp, WH, Chapman, ER, Sun, S, Johnson, EA
Montal, M
Liu, H, Tepp, WH, Chapman, ER, Sun, S, Suresh, S, Edwardson, JM, Johnson, EA
Koriazova, LK, Montal, M
protein transmembrane transporter activity of botB HC:LC:SYT:GT1b [synaptic vesicle membrane]
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