What type of macromolecule is botulinum toxin?
BoNT-A is synthesized as macromolecular protein complexes in nature. The progenitor toxins are known as protein complexes and consist of nontoxic accessory proteins (NAPs). The BoNT-A protein has a molecular weight of 150 kDa, and the NAP is associated to this active neurotoxin.
What is the shape of botulism?
Clostridium botulinum is an anaerobic, rod-shaped sporeforming bacterium that produces a protein with characteristic neurotoxicity.
What is the molecular target and effect of botulinum toxin?
The molecular targets of botulinum neurotoxins (BoNTs) are SNARE (soluble N-ethylmaleimide-sensitive factor-attachment protein-receptor) proteins necessary for neurotransmitter release. BoNT are powerful therapeutic agents in the treatment of numerous neurological disorders.
How do proteins affect botulinum toxin?
In conclusion, complexing proteins do not contribute to the stability of botulinum toxin type A drugs and do not contribute to their therapeutic effects, but may be associated with a secondary nonresponse due to the development of neutralizing antibodies.
Which part of the botulinum toxin molecule is responsible for binding the molecule to the pre synaptic cholinergic membrane?
[5] The heavy (H) chain of the toxin binds selectively and irreversibly to high affinity receptors at the presynaptic surface of cholinergic neurones, and the toxin-receptor complex is taken up into the cell by endocytosis.
How does botulinum toxin prevent normal motor neuron synaptic communication?
Synaptic vesicles fuse with the membrane in response to an elevation of intraneuronal calcium concentration and undergo release of their transmitter by exocytosis. Through their proteolytic action on these proteins, botulinum toxins prevent exocytosis, thereby inhibiting the release of acetylcholine.
Is botulinum toxin an exotoxin?
Proteinaceous ‘exotoxins’ such as tetanus, diphtheria, or botulinum toxins are typically secreted in contrast to ‘endotoxins’ that are bound to the bacterial body, and develop their pathogenic effects only after bacterial cell decay.