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XB-ART-38172
J Formos Med Assoc 2008 Aug 01;1078:600-8. doi: 10.1016/S0929-6646(08)60177-1.
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Effects of sodium azide, barium ion, d-amphetamine and procaine on inward rectifying potassium channel 6.2 expressed in Xenopus oocytes.

Kung FL , Tsai JL , Lee CH , Lou KL , Tang CY , Liou HH , Lu KL , Chen YH , Wang WJ , Tsai MC .


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Inward rectifying potassium channel 6.2 (Kir6.2DelataC26 channel) is closely related to ATP-sensitive potassium channels. Whether sodium azide, barium ion, d-amphetamine or procaine acts directly on the Kir6.2DeltaC26 channel remains unclear. We studied the effects of these compounds on Kir6.2DeltaC26 channel expressed in Xenopus oocytes. The coding sequence of a truncated form of mouse Kir6.2 (GenBank accession number NP_034732.1), Kir6.2(1-364) (i.e. Kir6.2DeltaC26), was subcloned into the pET20b(+) vector. Plasmid containing the correct T7 promoter-Kir6.2(1-364) cDNA fragment [Kir6.2/pET20b(+)] was then subject to NotI digestion to generate the templates for in vitro run-off transcriptions. The channel was expressed in Xenopus laevis oocytes. Two-electrode voltage clamping was used to measure the effects of sodium azide, barium ion, d-amphetamine and procaine on Kir6.2DeltaC26 channel current. Sodium azide activated and barium ion and d-amphetamine inhibited the Kir6.2DeltaC26 channel. Procaine did not have any significant effect on the Kir6.2DeltaC26 channel. Kir6.2DeltaC26 channel expressed in Xenopus oocytes can be used as a pharmacological tool for the study of inward rectifying potassium channels.

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Species referenced: Xenopus laevis
Genes referenced: kcnj11