Recombinant Conus kinoshitai Mu-conotoxin KIIIB, partial

Mu-conotoxin KIIIA-P1: mu-conotoxins block voltage-gated sodium channels (Nav). This toxin potently blocks Nav1.2/SCN2A (IC(50)~5 nM) and Nav1.4/SCN4A (IC(50)=20-90 nM). It moderately blocks Nav1.1/SCN1A, mNav1.6/SCN8A, and Nav1.7/SCN9A. It also shows a very low activity on Nav1.3/SCN3A. This toxin binds a microsite within the pore different from the tetrodotoxin binding site 1 (tested on Nav1.2). The block is partial, with a residual current that can be completely blocked by TTX. The toxin probably docks at a more superficial site in the outer vestibule of the channel than does TTX. On rNav1.2/SCN2A, it produces a block that is only partially reversible. The block of Nav1.7 is modified when beta-subunits are coexpressed with the alpha subunit. Hence, blocks of channels containing beta-1 and beta-3 subunits are more potent (compared to channels without beta subunits), whereas blocks of channels containing beta-2 and beta-4 subunits are less potent (compared to channels without beta subunits).; Mu-conotoxin KIIIA-P2: This toxin potently blocks Nav1.2/SCN2A (Kd=230 nM) and Nav1.4/SCN4A (Kd=830 nM). It also moderately blocks Nav1.7/SCN9A (Kd=1.57 uM). In addition, this toxin may also inhibit other sodium channels, as does Mu-conotoxin KIIIA-P1.; Mu-conotoxin KIIIB-P1: This toxin potently blocks Nav1.2/SCN2A (Kd=470 nM). In addition, this toxin may also inhibit other sodium channels, as does Mu-conotoxin KIIIA-P1.; Mu-conotoxin KIIIB-P2: This toxin potently blocks Nav1.2/SCN2A (Kd=26 nM). In addition, this toxin may also inhibit other sodium channels, as does Mu-conotoxin KIIIA-P1.