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

Research output: Contribution to journalArticlepeer-review

Abstract

Ca2+ entry (ICa) 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 ICa 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.

Original languageEnglish (US)
Pages (from-to)639-650
Number of pages12
JournalJournal of Molecular and Cellular Cardiology
Volume33
Issue number4
DOIs
StatePublished - 2001
Externally publishedYes

Keywords

  • Calmodulin binding domain
  • Calmodulin kinase
  • Facilitation
  • ICP domain
  • Inactivation
  • L-type Cachannels

ASJC Scopus subject areas

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine

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