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    Nanion Technologies: イオンチャネル研究のスマートツール

  • SyncroPatch 384i: HTS Automated Patch Clamp

    SyncroPatch 384i: HTS Automated Patch Clamp

  • SURFE²R 96SE: ラベルフリーのトランスポーターHTS

    SURFE²R 96SE: ラベルフリーのトランスポーターHTS

  • Dynamic Clamp: Patchliner

    Dynamic Clamp: Patchliner

  • 脂質二分子膜実験: Orbitシリーズ

    脂質二分子膜実験: Orbitシリーズ

  • CardioExcyte 96 SOL: 心筋の光ペーシング

    CardioExcyte 96 SOL: 心筋の光ペーシング

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SyncroPatch 384

SyncroPatch 384

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FLEXcyte 96

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SURFE²R N1

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Orbit 16 TC

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Vesicle Prep Pro

TASK-1 - "Activation and Inhibition of TASK-1 on Nanion’s SyncroPatch 384PE"

icon sp96   SyncroPatch 384PE (a predecessor model of SyncroPatch 384) application note:   logo pdf   (3.1 MB)
Cells were kindly provided by SB Drug Discovery.

Summary:

The resting membrane potential of excitable cells is determined by leak conductances predominantly mediated by KCNK and two-pore-domain potassium channels (K2P). K2P channels are characterized by the presence of two pore forming regions and four trans-membrane spanning (4TMS) regions in each channel subunit and form functional dimers. These channels are essential for the production of background leak type potassium currents that act to regulate resting membrane potential and levels of cellular excitability. The TWIKrelated acid-sensitive K+ channel 1 (K2P3.1 or TASK-1) is a member of the K2P channel family and is encoded by the KCNK3 gene. TASK-1 is ubiquitously expressed throughout the CNS but also in other tissues such as in the heart, adrenal gland, lung, pancreas,kidney, intestine and prostate. TASK-1 has been implicated in atrial fibrillation (AF) pathophysiology and was suggested as an atrial-selective antiarrhythmic drug target. TASK-1 is activated by extracellular acidosis and inhibited by anandamide and by local anesthetics including bupivicaine. Volatile general anestethics such as halothan and xenon stimulate TASK-1.

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