Evidence 1
Activity
Activity
Neurotoxin
FUNCTION: Mu-conotoxins block voltage-gated sodium channels (Nav). This synthetic toxin blocks both voltage-gated sodium channels and nicotinic acetylcholine receptor (nAChR). Inhibits the skeletal muscle rNav1.4/SCN4A (IC(50)=1.3 nM) and the brain rNav1.2/SCN2A in a long-lasting manner. A low inhibition is also observed on neuronal mNav1.6/SCN8A and mNav1.7/SCN9A. Modestly blocks nAChR alpha-3/beta-2 subtype (IC(50)=450 nM) (partially reversible) and, to a lesser extent, alpha-7 and alpha-4/beta-2 subtypes (reversible). In vitro, decreases twitch tension in mouse hemidiaphragms (IC(50)=150 nM), and displays a high blocking effect in mouse extensor digitorum longus muscles (IC(50)=46 nM). {ECO:0000269|PubMed:22229737}.
Target
nicotinic acetylcholine receptor (nAChR)
acetylcholine receptor
voltage-gated sodium channel (Nav)
Source & Reference
NA
UniProtKB/Swiss-Prot Tox-Prot
Other
Conus consors (Singed cone)
Neurotoxin
Postsynaptic neurotoxin
Acetylcholine receptor inhibiting toxin
Ion channel impairing toxin
Voltage-gated sodium channel impairing toxin
Mu-conotoxins block voltage-gated sodium channels (Nav). This synthetic toxin blocks both voltage-gated sodium channels and nicotinic acetylcholine receptor (nAChR).
Mu-conotoxin CnIIIC
cone snail
Conotoxin M superfamily
Evidence at protein level
3D-structure
Acetylcholine receptor inhibiting toxin
Amidation
Direct protein sequencing
Disulfide bond
Ion channel impairing toxin
Neurotoxin
Postsynaptic neurotoxin
Pyrrolidone carboxylic acid
Secreted
Toxin
Voltage-gated sodium channel impairing toxin
TISSUE SPECIFICITY: Expressed by the venom duct.