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Our Bioassay
- Jin, W. and Lu, Z. (1998) Biochemistry 37, 13291.
- Drici, M.D. et al. (2000) Br. J. Pharmacol. 131, 569.
- Kitamura, H. et al. (2000) Pharmacol. Exp. Therap. 293, 196.
- Alomone Labs Tertiapin inhibits Kir3.2 channels expressed in Xenopus oocytes.A continuous current trace recorded at a holding potential of -80 mV. Channel activation was achieved by high K+ solution perfusion. 50 nM Tertiapin (#STT-250) was applied during the period (2 minutes each) marked as a green trace.
- Jin, W. and Lu, Z. (1998) Biochemistry 37, 13291.
- Drici, M.D. et al. (2000) Br. J. Pharmacol. 131, 569.
- Kitamura, H. et al. (2000) J. Pharmacol. Exp. Therap. 293, 196.
- Jin, W. et al. (1999) Biochemistry 38, 14294.
Tertiapin is a 21 amino acid long toxin, originally isolated from Apis mellifera bee venom. Native and synthetic Tertiapin block a range of inward rectifier K+ channels. (Kir), in particular ROMK1 (Kir1.1, IC50 = 2 nM) and GIRK (Kir3 family, IC50 for the Kir3.1/3.4 heteromer is 8.6 nM) but with no effect on Kir2 family members1. In addition, it was shown to inhibit acetylcholine-induced K+ currents in the heart2,3.
Tertiapin is as active as Tertiapin-Q (#STT-170), a derivative of Tertiapin in which the oxidation-liable methionine is replaced by a glutamine residue4.
Tertiapin (#STT-250) is a highly pure, synthetic, and biologically active peptide toxin.
Applications
Specifications
Scientific Background
Citations
- Skov, J. et al. (2011) Cell. Mol. Neurobiol. 31, 587.
- Farhang, B. et al. (2010) Neuropharmacology 59, 190.
- Leuranguer, V. et al. (2008) Br. J. Pharmacol. 153, 57.
- Russo, M.J. et al. (2008) J. Neurophysiol. 100, 3351.
- Witkowski, G. et al. (2008) Neuroscience 155, 53.
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