Overview
- Jin, W. and Lu, Z. (1998) Biochemistry 37, 13291.
- Jin, W. et al. (1999) Biochemistry 38, 14294.
- Drici, M.D. et al. (2000) Br. J. Pharmacol. 131, 569.
- Kitamura, H. et al. (2000) Pharmacol. Exp. Ther. 293, 196.
Live cell imaging of Tertiapin-Q-ATTO Fluor-633 in differentiated PC-12 cells.Neurite outgrowth was induced in PC12 cells through a weak exposure to 100 ng/ml Native mouse NGF 2.5S protein (>95%) (#N-100). (A) CellMask™ Actin 1X solution was applied for 30 minutes, resulting in a green fluorescence to visualize cellular membrane. (B) Following this, the same cells underwent incubation with 1 µM of Tertiapin-Q-ATTO Fluor-633 for 30 minutes at 370C, followed by PBSX1 wash, leading to red fluorescence indicative of the distribution of inward rectifier K+ channels (Kir). (C) Live imaging of the differentiated PC-12 cells allowed observation of Tertiapin-Q distribution among the cells.
Unlabeled Tertiapin-Q successfully blocks Kir channels access.(A) Live imaging of the differentiated PC-12 cells allowed observation of Tertiapin-Q-ATTO Fluor-633 (0.5 µM) distribution among the cells. (B) Live imaging of differentiated PC-12 cells demonstrates that Tertiapin-Q (#STT-170, 5 µM) successfully competes with Tertiapin-Q-ATTO Fluor-633 (0.5 µM) for binding sites of Kir channels. (Cells underwent incubation for 15 minutes at 370C).
Direct flow cytometry of Tertiapin-Q in live intact rat PC-12 cells.___ PC-12 cells.
___ PC-12 cells + 50 nM Tertiapin-Q (#STT-170).
___ PC-12 cells + 50 nM Tertiapin-Q-ATTO Fluor-633 (#STT-170-FR).
Alomone Labs Tertiapin-Q-ATTO Fluor-633 inhibits Kir3.2 channel heterologously expressed in Xenopus oocytes.A continuous current trace recorded at a holding potential of -80 mV. Kir3.2 currents are downward reflections activated by high K+ containing solution. While activated, 50 nM and 100 nM of Tertiapin-Q-ATTO Fluor-633 (#STT-170-FR) were applied for 2 min (indicated as bars).
- 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. Ther. 293, 196.
- Peleg, S. et al. (2002) Neuron 33, 87.
- Kanjhan, R. et al. (2005) J. Pharmacol. Exp. Ther. 314, 1353.
Tertiapin, the native toxin, was originally isolated from European honey bee Apis mellifera venom. Native and synthetic Tertiapin blocks 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 was 8.6 nM) but with no effect on the Kir2 family member1. In accordance, it was shown to inhibit acetylcholine induced K+ currents in mammalian cardiomyocytes2,3.
Tertiapin-Q is a derivative of Tertiapin in which Met13 is substituted by a Gln residue. However, unlike native Tertiapin, Tertiapin-Q is non-oxidizable and therefore is more stable4.
Tertiapin-Q inhibits the above-mentioned channels with similar affinities and also inhibits Ca2-activated large conductance BK-type K+ channels in a concentration and voltage-dependent manner5.
Tertiapin-Q-ATTO Fluor-633 (#STT-170-FR) is a highly pure, synthetic, and biologically active conjugated peptide toxin.
✓ Live cell imaging
✓ Single cell detection
✓ Direct flow cytometry
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