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Biological Activity for ShK-Dap22
ShK-Dap22 is an extremely potent KV1.3 channel blocker (Kd = 23 pM for mKV1.3 currents). Selective for KV1.3 over other mammalian potassium channels (IC50 values are 23, 1800, 10500, 37000 and 39000 pM for mKV1.3, mKV1.1, hKV1.6, mKV1.4 and rKV1.2 respectively, and >100000 pM for hKV1.5, mKV1.7, hKV3.1, rKV3.4 and hKCa4). Suppresses T cell activation in vitro (IC50 < 500 pM).
Technical Data for ShK-Dap22
(Modifications: Disulfide bridges: 3-35,12-28,17-32), X= Dap)
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Solubility Data for ShK-Dap22
|Solubility||Soluble to 1 mg/ml in water|
References for ShK-Dap22
References are publications that support the biological activity of the product.
Kalman et al (1998) ShK-Dap22, a potent KV1.3-specific immunosuppresive polypeptide. J.Biol.Chem. 273 32697 PMID: 9830012
Robbins et al (2005) Hypoxia modulates early events in T cell receptor-mediated activation in human T lymphocytes via KV1.3 channels. J.Physiol. 564 131 PMID: 15677684
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Citations for ShK-Dap22
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Reviews for ShK-Dap22
Average Rating: 5 (Based on 1 Review.)
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
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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.