4.5 Article

Ca2+-dependent regulation of cardiac L-type Ca2+ channels:: is a unifying mechanism at hand?

期刊

出版社

ELSEVIER SCI LTD
DOI: 10.1006/jmcc.2000.1354

关键词

L-type Ca2+ channels; facilitation; inactivation; calmodulin kinase; ICP domain; calmodulin binding domain

资金

  1. NHLBI NIH HHS [HL03727, HL62494] Funding Source: Medline

向作者/读者索取更多资源

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.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.5
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据