Suppression of inward-rectifying K+ channels KAT1 and AKT2 by dominant negative point mutations in the KAT1 α-subunit

V. M. Baizabal-Aguirre, S. Clemens, Nobuyuki Uozumi, J. I. Schroeder

研究成果: Article査読

57 被引用数 (Scopus)

抄録

The Arabidopsis thaliana cDNA, KAT1 encodes a hyperpolarization- activated K+ (K+(in)) channel. In the present study, we identify and characterize dominant negative point mutations that suppress K+(in) channel function. Effects of two mutations located in the H5 region of KAT1, at positions 256 (T256R) and 262 (G262K), were studied. The co-expression of either T256R or G262K mutants with KAT1 produced an inhibition of K+ currents upon membrane hyperpolarization. The magnitude of this inhibition was dependent upon the molar ratio of cRNA for wild-type to mutant channel subunits injected. Inhibition of KAT1 currents by the co-expression of T256R or G262K did not greatly affect the ion selectivity of residual currents for Rb+, Na+, Li+, or Cs+. When T256R or G262K were coexpressed with a different K+ channel, AKT2, an inhibition of the channel currents was also observed. Voltage-dependent Cs+ block experiments with co-expressed wild type, KAT1 and AKT2, channels further indicated that KAT1 and AKT2 formed heteromultimers. These data show that AKT2 and KAT1 are able to co-assemble and suggest that suppression of channel function can be pursued in vivo by the expression of the dominant negative K+(in) channel mutants described here.

本文言語English
ページ(範囲)119-125
ページ数7
ジャーナルJournal of Membrane Biology
167
2
DOI
出版ステータスPublished - 1999 2 9
外部発表はい

ASJC Scopus subject areas

  • 生物理学
  • 生理学
  • 細胞生物学

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