Recombinant Conus kinoshitai Mu-conotoxin KIIIB, partial

SKU: P0C195

Size: 100ug. Other sizes are also available.

Activity: Not tested

Research Areas: Others

Uniprot ID: P0C195

Gene Names: N/A

Alternative Name(s):

Abbreviation: Recombinant Conus kinoshitai Mu-conotoxin KIIIB protein, partial

Organism: Conus kinoshitai (Kinoshita's cone)

Source: Yeast

Expression Region: 5-20aa

Protein Length: Partial

Tag Info: N-terminal 6xHis-sumostar-tagged

Target Protein Sequence: CCNCSSKWCRDHSRCC

MW: 15.0 kDa

Purity: Greater than 90% as determined by SDS-PAGE.

Endotoxin: Not test

Biological_Activity:

Form: Liquid or Lyophilized powder

Buffer: If the delivery form is liquid, the default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol. If the delivery form is lyophilized powder, the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, pH 8.0.

Reconstitution: We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20℃/-80℃. Our default final concentration of glycerol is 50%. Customers could use it as reference.

Storage: The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself. Generally, the shelf life of liquid form is 6 months at -20℃/-80℃. The shelf life of lyophilized form is 12 months at -20℃/-80℃.

Notes: Repeated freezing and thawing is not recommended. Store working aliquots at 4℃ for up to one week.

Relevance: Mu-conotoxin KIIIA-P1: mu-conotoxins block voltage-gated sodium channels (Nav). This toxin potently blocks Nav1.2/SCN2A (IC(50)5-124 nM), Nav1.4/SCN4A (IC(50)=20-90 nM), and Nav1.7/SCN9A (IC(50)=290-413 nM). It moderately blocks Nav1.1/SCN1A, and mNav1.6/SCN8A. 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, IC(50)=1.37 uM) and Nav1.4/SCN4A (Kd=830 nM, IC(50)=2 uM). It also moderately blocks Nav1.7/SCN9A (Kd=1.57 uM, IC(50)=5.4 uM). In addition, this toxin may also inhibit other sodium channels, as does Mu-conotoxin KIIIA-P1. ; Mu-conotoxin KIIIA-N: This toxin moderately blocks Nav1.2/SCN2A (IC(50)=875 nM), Nav1.4/SCN4A (IC(50)=472 nM), and Nav1.7/SCN9A (IC(50)=887 nM). ; 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.

Reference:

Function: