Antisense oligonucleotides against receptor kinase GRK2 disrupt target selectivity of β-adrenergic receptors in atrial myocytes

被引：16

作者：

Wellner-Kienitz, MC ^{[1
]}

Bender, K ^{[1
]}

Brandts, B ^{[1
]}

Meyer, T ^{[1
]}

Pott, L ^{[1
]}

机构：

[1] Ruhr Univ Bochum, Inst Physiol, Abt Zellulare Physiol, D-44780 Bochum, Germany

来源：

FEBS LETTERS | 1999年 / 451卷 / 03期

关键词：

potassium channel; GIRK; G-protein; beta-receptor; GRK2; antisense;

D O I：

10.1016/S0014-5793(99)00594-3

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

K+ channels composed of GIRK subunits are predominantly expressed in the heart and various regions of the brain, They are activated by beta gamma-subunits released from pertussis toxin-sensitive G-proteins coupled to different seven-helix receptors, In rat atrial myocytes, activation of K-(ACh) channels is strictly limited to receptors coupled to pertussis toxin-sensitive G-proteins. Upon treatment of myocytes with antisense oligodesoxynucleotides against GRK2, a receptor kinase with G(beta gamma) binding sites, in a fraction of cells, K-(ACh) channels can be activated by beta-adrenergic receptors, Sensitivity to beta-agonist is insensitive to pertussis toxin treatment. These findings demonstrate a potential role of G(beta gamma) binding proteins for target selectivity of G-protein-coupled receptors. (C) 1999 Federation of European Biochemical Societies.

引用

页码：279 / 283

页数：5

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