L-type Ca2+ channels in Ca2+ channelopathies

被引：30

作者：

Striessnig, J ^{[1
]}

Hoda, JC ^{[1
]}

Koschak, A ^{[1
]}

Zaghetto, F ^{[1
]}

Müllner, C ^{[1
]}

Sinnegger-Brauns, MJ ^{[1
]}

Wild, C ^{[1
]}

Watschinger, K ^{[1
]}

Trockenbacher, A ^{[1
]}

Pelster, G ^{[1
]}

机构：

[1] Univ Innsbruck, Inst Pharm, Dept Pharmacol & Toxicol, A-6020 Innsbruck, Austria

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2004年 / 322卷 / 04期

基金：

奥地利科学基金会;

关键词：

D O I：

10.1016/j.bbrc.2004.08.039

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：

Voltage-gated L-type Ca2+ channels (LTCCs) mediate depolarization induced Ca2+ entry in electrically excitable cells, including muscle cells, neurons, and endocrine and sensory cells. In this review we summarize the role of LTCCs for human diseases caused by genetic Ca2+ channel defects (channelopathies). LTCC dysfunction can result from structural aberrations within pore-forming alphal subunits causing incomplete congenital stationary night blindness, malignant hyperthermia sensitivity or hypokalemic periodic paralysis. However, studies in mice revealed that LTCC dysfunction also contributes to neurological symptoms in Ca2+ channelopathies affecting non-LTCCs, such as Ca(v)2.1 alphal in tottering mice. Ca2+ channelopathies provide exciting molecular tools to elucidate the contribution of different LTCC isoforms to human diseases. (C) 2004 Published by Elsevier Inc.

引用

页码：1341 / 1346

页数：6

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