Kv2.1 and Kv2.2 channel blocker (IC50 values are 1-3 nM). Enhances glucose-stimulated insulin secretion from human islets in vitro, but not from islet cells lacking the Kv2.1 channel. Has no significant effect on plasma insulin, glucagon or blood glucose levels in mice, but increases plasma somatostatin levels.
(Modifications: Disulfide bridge: 4-19,11-24,18-31)
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
|Solubility||Soluble to 1 mg/ml in water|
References are publications that support the biological activity of the product.
Li et al (2013) The role of voltage-gated potassium channels Kv2.1 and Kv2.2 in the regulation of insulin and somatostatin release from pancreatic islets. J.Pharmacol.Exp.Ther. 344 407 PMID: 23161216
Herrington (2007) Gating modifier peptides as probes of pancreatic beta-cell physiology. Toxicon 49 231 PMID: 17101164
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Literature in this Area
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Epilepsy is a brain disease that affects 60 million people globally. More than 20 anti-seizure drugs are currently available, but these do not address the underlying causes of the condition. This poster summarizes current knowledge about the development of the condition and highlights some approaches that have disease-modifying effects in proof-of-concept studies.
Peripheral sensitization is the reduction in the threshold of excitability of sensory neurons that results in an augmented response to a given external stimulus. This poster outlines the excitatory and inhibitory signaling pathways involved in modulation of peripheral sensitization. The role of ion channels, GPCRs, neurotrophins, and cytokines in sensory neurons are also described.