Botulinum toxin type G (botG) is rarely if ever associated with human disease (Hatheway 1995) and a pathway by which it might enter the circulation from the human gut has not been described. Nevertheless, the toxin itself, a disulfide-bonded heavy chain (HC) - light chain (LC) heterodimer ("dichain"), is capable of binding to neurons by interactions with cell-surface ganglioside and syntagmin 1 (SYT1) (Peng et al. 2012; Willjes et al. 2013), the bound toxin can enter synaptic vesicles and release its LC moiety into the cytosol of targeted cells (Montal 2010), and the botG LC can cleave vesicle-associated membrane proteins 1 and 2 (VAMP1 and 2) on the cytosolic face of the synaptic vesicle membrane (Schiavo et al. 1994; Yamasaki et al. 1994). These four events are annotated here.
Yamasaki, S, Binz, T, Hayashi, T, Szabo, E, Yamasaki, N, Eklund, M, Jahn, R, Niemann, H
Willjes, G, Mahrhold, S, Strotmeier, J, Eichner, T, Rummel, A, Binz, T
Peng, L, Berntsson, RP, Tepp, WH, Pitkin, RM, Johnson, EA, Stenmark, P, Dong, M
Montal, M
Schiavo, G, Malizio, C, Trimble, WS, Polverino de Laureto, P, Milan, G, Sugiyama, H, Johnson, EA, Montecucco, C
Hatheway, CL
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