Alterations in conserved Kir channel-PIP2 interactions underlie channelopathies

被引：330

作者：

Lopes, CMB

Zhang, HL

Rohacs, T

Jin, TH

Yang, J

Logothetis, DE ^{[1
]}

机构：

[1] NYU, Mt Sinai Sch Med, Dept Physiol & Biophys, New York, NY 10029 USA

[2] Hebei Med Univ, Dept Pharmacol, Shijiazhuang, Peoples R China

[3] Columbia Univ, Dept Biol Sci, New York, NY 10027 USA

来源：

NEURON | 2002年 / 34卷 / 06期

关键词：

D O I：

10.1016/S0896-6273(02)00725-0

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Inwardly rectifying K+ (Kir) channels are important regulators of resting membrane potential and cell excitability. The activity of Kir channels is critically dependent on the integrity of channel interactions with phosphatidylinositol 4,5-bisphosphate (PlP(2)). Here we identify and characterize channel-PIP2 interactions that are conserved among Kir family members. We find basic residues that interact with PIP2, two of which have been associated with Andersen's and Bartter's syndromes. We show that several naturally occurring mutants decrease channel-PIP2 interactions, leading to disease.

引用

收藏

页码：933 / 944

页数：12

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