Centrifuge the vial (10,000 x g for 5 minutes) before adding solvent to spin down all the powder to the bottom of the vial. The lyophilized product may be difficult to visualize. Add solvent directly to the centrifuged vial. Gently tap, tilt, and roll the vial to aid dissolution. Avoid vigorous vortexing, light vortexing for up to 3 seconds is acceptable if needed. The product is soluble in pure water at high micromolar concentrations (100 μM - 1 mM). For long-term storage in solution, we recommend preparing a stock solution by dissolving the product in double-distilled water (ddH2O) at a concentration between 100-1000x of the final working concentration. Divide the stock solution into small aliquots and store at -20 °C. Before use, thaw the relevant vial(s) and dilute to the desired working concentration in your working buffer. Centrifuge all product preparations before use. It is recommended to prepare fresh solutions in working buffers just before use. Avoid multiple freeze-thaw cycles to maintain biological activity.
Buffer
Lyophilized from double distilled water (ddH2O). May contain TFA as a residual counter ion.
Lagerung
4 °C,-20 °C
Informationen zur Lagerung
The reconstituted solution can be stored at 4°C for up to 1 week. For longer periods (up to 6 months), small aliquots should be stored at -20°C. We do not recommend storing the product in working solutions for longer than a few days. Avoid multiple freeze-thaw cycles.,The reconstituted solution can be stored at 4°C for up to 1 week. For longer periods (up to 6 months), small aliquots should be stored at -20°C. We do not recommend storing the product in working solutions for longer than a few days. Avoid multiple freeze-thaw cycles.
Target
alpha-conotoxin GI
Hintergrund
α-Conotoxin G1, Alpha-conotoxin GI,α-Conotoxin GI is a 13 amino acid peptidyl toxin isolated from the Conus geographus (Geography cone) venom1,2,3. It belongs to the Conotoxin A superfamily and reversibly blocks α/δ nicotinic ACh channel receptors (nAChR).α-Conotoxin GI reversibly inhibits the high affinity α/δ site on mouse muscle-derived BC3H-1 receptor, a nAChR expressed on postsynaptic membranes4,5. Other low site (α/γ site) on nicotinic receptors from Torpedo californica electric organ is also inhibited by α-Conotoxin GI5.