Evidence 1
Activity
Activity
Neurotoxin
FUNCTION: Mu-conotoxins block voltage-gated sodium channels (Nav). This synthetic toxin potently blocks rNav1.4/SCN4A (IC(50)= 7 nM). It also moderately blocks rNav1.1/SCN1A (IC(50)=370 nM), rNav1.2/SCN2A (IC(50)=1 uM), and mNav1.6/SCN6A (IC(50)=570 nM) (PubMed:18831583, PubMed:21652775). It is noteworthy that coexpression of subunits beta-2 or beta-4 (but not beta-1 or beta-3) decrease by more that 10-fold the binding potency of the toxin to rNav1.6 (PubMed:25632083). It is also noteworthy that the toxin is 50-fold more potent on mouse Nav1.6 than on rat Nav1.6 (PubMed:25632083). In vivo, when injected intraperitoneally or subcutaneously in mice, causes motor impairment, paralysis and death (PubMed:18831583). {ECO:0000269|PubMed:18831583, ECO:0000269|PubMed:21652775}.
Target
voltage-gated sodium channel (Nav)
Source & Reference
NA
UniProtKB/Swiss-Prot Tox-Prot
Other
Conus striolatus (Cone snail)
Neurotoxin
Ion channel impairing toxin
Voltage-gated sodium channel impairing toxin
Mu-conotoxins block voltage-gated sodium channels (Nav). This synthetic toxin potently blocks rNav1.4/SCN4A (IC(50)= 7 nM).
Mu-conotoxin SxIIIA
cone snail
Conotoxin M superfamily
Evidence at protein level
Amidation
Disulfide bond
Ion channel impairing toxin
Neurotoxin
Secreted
Toxin
Voltage-gated sodium channel impairing toxin
TISSUE SPECIFICITY: Expressed by the venom duct. {ECO:0000305|PubMed:18831583}.