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Mipartoxin-I is a neurotoxin produced by the Micrurus mipartitus, a coral snake from Nicaragua. It causes a neuromuscular blockade via a post-synaptic action through the cholinergic nicotinic receptor.

Source
The toxin is produced by the Micrurus mipartitus, also known as ‘redtail coral snake’, ‘rabo de ají’, or ‘gargantilla’.[1] The snake populates Nicaragua, Costa Rica, isthmus of Panama, Ecuador, Colombia, and Venezuela.

Structure and family
Mipartoxin-I is a short-chain, type-I, α-neurotoxin composed of 60 amino acids. It is a member from the three finger toxin (3FTx) superfamily. Presence of eight cysteines in the amino acid sequence is a characteristic of mipartoxin-I, as well as a characteristic of the 3FTx superfamily. Similar to other proteins of this family, mipartoxin-I is a basic protein. Compared to other proteins of this family, considerable differences has been shown, but no identity values higher than 70% were found. However, most of the other proteins have identity values within the range of 25-55%. Mipartoxin-I has an observed mass of 7030.0.[1]

Homology
The structural model of CTX A5, a cardiotoxin from the Cobra Naja atra, shows similarities with mipartoxin-I in core and in amino acid sequence identity (38%). However, there are some slight differences in loop 2, and major differences in loop 3.[1]

Structural model of CTX A5 (grey) compared to the structural model of mipartoxin-I (red).[1]

Target
Mipartoxin-I antagonistically binds to the nicotinic acetylcholine receptors. The toxin blocks the contractures of the muscles, but it does not interfere with the presynaptic mechanisms of neurotransmitter release. This indicates that mipartoxin-I causes a blockade via a post-synaptic action.[1] Thus, mipartoxin-I inhibits the activity of the acetylcholine receptor, without damaging the muscle fibres.[2]

Toxicity
Envenoming causes bilateral ptosis and progressive respiratory paralysis. Following a decrease in activity and respiratory paralysis, mice die a few hours after envenoming. LD50 of mice is 0.06 μg/g body weight.[1][2]

Treatment
Currently, no specific antivenom is available in most of its important geographic field (Central America). The scarcity of an antivenom is complicated by insufficient cross-protection by antivenoms that are more accessible in this geographic area. However, identity values of related toxin of two South American coral snakes were high (M. frontalis 70% and M. altirostris 68%). This indicates a possible cross-protection of these two antivenoms for mipartoxin-I.[1]