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- Diochot, S. et al. (1998) J. Biol. Chem. 273, 6744.
- Liu, P. et al. (2012) J. Neurophysiol. 107, 3155.
- Alomone Labs BDS-I enhances the current of NaV1.7 channels expressed in Xenopus oocytes.A. Time course of BDS-I (#STB-400) effect on the normalized area of NaV1.7 channel current. Membrane potential was held at -100 mV, current was elicited by a 100 ms voltage step to 0 mV every 1 sec, and was significantly enhanced by 3.5 min application of 100 nM BDS-I, indicated by the horizontal bar. B. Superimposed traces of NaV1.7 current upon application of control and of 100 nM BDS-I (as indicated), taken from the recording shown in A.
- Diochot, S. et al. (1998) J. Biol. Chem. 273, 6744.
- Yeung, S.Y. et al. (2005) J. Neurosci. 25, 8735.
- Kaab, S. et al. (2005) J. Physiol. 566, 395.
- Baranauskas, G. et al. (2004) Nature Neurosci. 6, 258.
- Shevchenko, T. et al. (2004) J. Neurophysiol. 92, 3043.
- Wang, L. et al. (2004) Invest. Ophthamol. Vis. Sci. 45, 1796.
- Sanchez, D. et al. (2002) J. Physiol. 542, 369.
- Riazanski, V. et al. (2001) J. Physiol. 537, 391.
- Liu, P. et al. (2012) J. Neurophysiol. 107, 3155.
BDS-I is a 43 amino acid peptidyl toxin isolated from the sea anemone Anemonia sulcata venom. It is reported to be a selective blocker of KV3.4 K+ channel. BDS-I blocks 60% of the KV3.4 current in COS-transfected cells at a concentration of 2.5 µM. The blocking effect is rapid, direct and reversible1. Recently it was shown that it blocks other KV3 channels with similar potencies2.
BDS-I inhibits KV currents in carotid body cells3, an effect which disappears after chronic hypoxia, establishing the unique role played by KV3 channels in the response to hypoxia4. BDS-I (2.5 µM) also reduces the native transient K+ current and increases the action potential duration in hippocampal granule neurons5. In corneal epithelial cells BDS-I (400 nM) inhibits most of the detected KV current6. In magnocellular neurosecretory neurons of the hypothalamus, 100 nM BDS-I inhibits about half of the KV current and increases the action potential duration7. In fast spiking neurons from different brain areas, 2 µM BDS-I inhibits part of the KV current and broadened the action potential and reduces spike frequency8.
BDS-I also produces broadening of the spike and accelerates the upstroke of the action potential by modulating voltage-gated Na+ channels. It enhances TTX-sensitive Na+ channels (highly effective on NaV1.7 channels), and weakly inhibits TTX-resistant NaV channels9.
BDS-I (#STB-400) is a highly pure, synthetic, and biologically active peptide toxin.
Applications
Citations
- Strege, P.R. et al. (2017) Sci. Rep. 7, 15650.
- Meneses, D. et al. (2016) Neural Plast. 2016, 8782518.
- Ubels, J.L. et al. (2016) Exp. Eye Res. 145, 26.
- Liu, P. et al. (2012) J. Neurophysiol. 107, 3155.
- Alle, H. et al. (2011) J. Neurosci. 31, 8001.
- Kanyshkova, T. et al. (2011) Pflugers Arch. 461, 545.
- Martel, P. et al. (2011) PLoS ONE 6, e20402.
- Min, M.Y. et al. (2010) Neuroscience 168, 633.
- Wu, Z.Z. et al. (2009) J. Biol. Chem. 284, 36453.
- Dallas, M.L. et al. (2008) Brain Res. 1189, 51.
Specifications
Scientific Background
Related Products
Antibodies
- Anti-KV3.1b (KCNC1) Antibody (#APC-014)
- Anti-KV3.2 (KCNC2) Antibody (#APC-011)
- Anti-KCNC3 (KV3.3) Antibody (#APC-102)
- Anti-KCNC4 (KV3.4) Antibody (#APC-019)
- Anti-NaV1.7 (SCN9A) Antibody (#ASC-008)
- Anti-NaV1.7 (SCN9A)-ATTO Fluor-633 Antibody (#ASC-008-FR)
- Guinea pig Anti-NaV1.7 (SCN9A) Antibody (#ASC-008-GP (formerly AGP-057))
- Anti-NaV1.7 (SCN9A) (extracellular) Antibody (#ASC-027)
Pharmacological tools
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