TCID | Name | Domain | Kingdom/Phylum | Protein(s) |
---|---|---|---|---|
1.C.8.1.1 | Botulinum neurotoxin types A-G. Poly(amindo)amine (PAMAM) detrimers block activity (Förstner et al. 2014). BoNTs inhibit synaptic exocytosis; intoxication requires the di-chain protein to undergo conformational changes in response to pH and redox gradients across the endosomal membrane with consequent formation of a protein-conducting channel by the heavy chain (HC) that translocates the light chain (LC) protease into the cytosol, colocalizing it with the substrate SNARE proteins (Montal 2009). Botulinum toxin type A inhibits salivary secretion, possibly by alterring RNA synthesis (Mao et al. 2020). | Bacteria |
Firmicutes | Botulinum neurotoxin precursor, type A of Clostridium botulinum |
1.C.8.1.2 | Tetanus neurotoxin | Bacteria |
Firmicutes | Tetanus neurotoxin precursor of Clostridium tetani |
1.C.8.1.3 | Clostridium botulinum neurotoxin type E (3d structure known (Kumaran et al., 2009)) | Bacteria |
Firmicutes | BoNTE of Clostridium botulinum (Q00496) |
1.C.8.1.4 | Non-toxic nonhemagglutinin type C of 1196 aas. Assembles with botulinum neurotoxin type C (BoNT/C) and protects it against pH-mediated inactivation or protease activity at pH 2.6 (the pH of the animal gastrointestinal tract) but not at pH 6.0. The non-toxic component is necessary to maintain toxicity. | Viruses |
Caudovirales | Nonhemagglutinin type C of Clostridium botulinum C phage (Clostridium botulinum C bacteriophage) |