Ca2+-dependent regulation of cardiac L-type Ca2+ channels: is a unifying mechanism at hand?
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.
Anderson
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ME
Department of Internal Medicine, Vanderbilt University, Nashville, Tennessee 37232, USA. mark.anderson@mcmail.vanderbilt.edu
D000595:Amino Acid Sequence; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D020746:Calcium Channels, L-Type / Q000378:metabolism* / Q000502:physiology; D002413:Cations, Divalent; D006801:Humans; D008969:Molecular Sequence Data
D020746:Calcium Channels, L-Type; D002413:Cations, Divalent; D002118:Calcium