Anderson M E
Department of Internal Medicine, Vanderbilt University, Nashville, Tennessee 37232, USA.
J Mol Cell Cardiol. 2001 Apr;33(4):639-50. doi: 10.1006/jmcc.2000.1354.
Ca2+ entry (I(Ca)) through cardiac L-type Ca2+ channels (LTCC) drives critical cellular processes ranging from contraction to gene expression, and, when disordered, is implicated in arrhythmias and hypertrophy. LTCC activation occurs by cell membrane depolarization, but LTCCs are also regulated by auxiliary proteins, phosphorylation, and intracellular CA2+([Ca2+]i). LTCC regulation by [Ca2+]i is especially intriguing because increased [Ca2+]i signals dual and conflicting commands for I(Ca)inactivation and facilitation. A recent explosion of work has shed new light on the mechanisms and molecular identity of domains necessary for [Ca2+]i-dependent regulation of LTCC.
通过心脏L型钙通道（LTCC）的Ca2+内流（I(Ca)）驱动着从收缩到基因表达等关键细胞过程，当其失调时，与心律失常和肥大有关。LTCC的激活通过细胞膜去极化发生，但LTCC也受辅助蛋白、磷酸化和细胞内Ca2+（[Ca2+]i）的调节。[Ca2+]i对LTCC的调节尤其引人关注，因为[Ca2+]i增加对I(Ca)的失活和易化发出了双重且相互矛盾的指令。最近大量的研究工作为[Ca2+]i依赖性LTCC调节所需结构域的机制和分子特性带来了新的认识。
