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 language | English (US) |
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Pages (from-to) | 639-650 |
Number of pages | 12 |
Journal | Journal of Molecular and Cellular Cardiology |
Volume | 33 |
Issue number | 4 |
DOIs | |
State | Published - 2001 |
Externally published | Yes |
Keywords
- Calmodulin binding domain
- Calmodulin kinase
- Facilitation
- ICP domain
- Inactivation
- L-type Cachannels
ASJC Scopus subject areas
- Molecular Biology
- Cardiology and Cardiovascular Medicine