The intrinsic gating of inward rectifier K+ channels expressed from the murine IRK1 gene depends on voltage, K+ and Mg2

1. We describe the cloning of the inward rectifier K+ channel IRK1 from genomic DNA of mouse; the gene is intronless. 2. The IRK1 gene can be stably expressed in murine erythroleukaemia (MEL) cells. Such transfected cells show inward rectification under whole-cell recording. 3. Channels encoded by t...

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Published inThe Journal of physiology Vol. 475; no. 1; pp. 1 - 7
Main Authors Stanfield, P R, Davies, N W, Shelton, P A, Khan, I A, Brammar, W J, Standen, N B, Conley, E C
Format Journal Article
LanguageEnglish
Published Oxford The Physiological Society 15.02.1994
Blackwell
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Summary:1. We describe the cloning of the inward rectifier K+ channel IRK1 from genomic DNA of mouse; the gene is intronless. 2. The IRK1 gene can be stably expressed in murine erythroleukaemia (MEL) cells. Such transfected cells show inward rectification under whole-cell recording. 3. Channels encoded by the IRK1 gene have an intrinsic gating that depends on voltage and [K+]o. Rate constants are reduced e-fold as the driving force on K+(V-EK) is reduced by 24.1 mV. 4. Removal of intracellular Mg2+ permits brief outward currents under depolarization. The instantaneous current-voltage relation may be fitted by an appropriate constant field expression. 5. Removal of intracellular Mg2+ speeds channel closure at positive voltages. In nominally zero [Mg2+]i, rate constants for the opening and closing of channels, processes which are first order, are similar to those of native channels.
Bibliography:ObjectType-Article-1
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content type line 23
ISSN:0022-3751
1469-7793
DOI:10.1113/jphysiol.1994.sp020044