Structural and functional derivations of each toxin type
Toxin type | Derivations |
|---|---|
| 3FTx | Basal activity of α-neurotoxicity greatly potentiated by the deletion of the C2 and C3 ancestral cysteines. Functional derivations include binding to the postsynaptic muscarinic acetylcholine receptors, presynaptic neurotoxic action upon the L-type calcium channels, cytotoxic interactions, acetylcholinesterase inhibition, and others. |
| Acetylcholinesterase | None currently documented. |
| ADAM | Prothrombin activation a basal derivation. In Viperidae venoms, proteolytic cleavage of C-terminal domains resulted in myriad of other activities including direct-acting fibrinolytic activity. Liberated disintegrin domain inhibits platelets via GP IIb/IIIa integrin receptor. |
| BNP | Cardiovascular effects independent of the GC-A receptor. Antiplatelet activities evolved for domains upstream of the natriuretic peptide domain. |
| CVF | None currently documented. |
| CNP-BPP | None currently documented. |
| CRISP | Blockage of cyclic nucleotide gated calcium channels. |
| Crotamine | Significant neurotoxic activity, modifying voltage-sensitive Na+ channels, resulting in a potent analgesic effect. |
| Cystatin | None currently documented. |
| Factor V | None currently documented. |
| Factor X | None currently documented. |
| Kallikrein | Derivations affect the blood, particularly targeting fibrinogen. |
| Kunitz | Derivations include inhibition of plasmin and thrombin and the blockage of L-type calcium channels. Structural derivatives form part of neurotoxic complexes with PLA2 molecules. |
| L-amino oxidase | Derivations include hemorrhagic effects, not only by affecting platelet aggregation, but also inhibiting blood factor IX. |
| Lectin | Derivations include stimulation of platelet aggregation (binding GPVI, GPIb, GPIa/IIa or VWF), platelet aggregation inhibition (binding GPIb or GPIa/IIa) or anticoagulant actions by binding blood factors IX, X. |
| MIT | None currently documented. |
| NGF | Immunomodulatory effects mediated through histamine release and plasma extravasation. |
| PLA2 (type IB) | Deletion of pancreatic loop facilitated the derivation of a multiplicity of novel, nonenzymatic activities, including antiplatelet and presynaptic neurotoxicity. Some derivatives are parts of neurotoxic complexes. |
| PLA2 (type IIA) | Derivations include neurotoxic and antiplatelet activity. Some derivatives are parts of complexes. |
| Sarafotoxin | None currently documented. |
| SPRY | None currently documented. |
| VEGF | Sustained hypotension. |
| Wagerlin | None currently documented. |
| Waprin | None currently documented. |