Ca2+-dependent regulation of cardiac L-type Ca2+ channels:: is a unifying mechanism at hand?
Ca2+-dependent regulation of cardiac L-type Ca2+ channels:: is a unifying mechanism at hand?
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DOI：
10.1006/jmcc.2000.1354
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发表时间：
2001-04-01
影响因子：
5
通讯作者：
Anderson, ME
中科院分区：
文献类型：
--
作者：
Anderson, ME
通过心脏L型Ca 2+通道（LTCC）的Ca 2+内流（I-Ca）驱动从收缩到基因表达的关键细胞过程，并且。当其紊乱时，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也受辅助蛋白的调节。磷酸化和细胞内Ca 2+（[Ca 2 +]（i））。[Ca 2 +]（i）对LTCC的调节特别有趣，因为增加的[Ca 2 +]（i）发出I-Ca失活和易化的双重和冲突的命令。最近的爆炸性的工作已经揭示了新的光的机制和分子身份的结构域所需的[Ca 2 +]（i）-依赖性调节LTCC。(C)北京：科学出版社.
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. (C) 2001 Academic Press.