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Voltage-dependent L-type calcium channel subunit alpha-1C (CaV1.2 or CACNA1C (for the gene)/CaV1.2 (for the protein))

Target
CaV1.2 or CACNA1C (for the gene)/CaV1.2 (for the protein)
Molecular classification
Ion channel, Voltage-gated calcium channel, L-type calcium channel
01

Overview

The voltage-dependent L-type calcium channel subunit alpha-1C (also known as CaV1.2, encoded by the CACNA1C gene) is a pore-forming subunit of the L-type calcium channel complex. This protein is responsible for mediating the influx of calcium ions into cardiac, smooth, and some neuronal cells upon membrane depolarization, triggering critical processes such as muscle contraction, hormone secretion, and gene expression. It is the principal target for the clinically important class of calcium channel-blocking drugs used primarily in treating cardiovascular disorders. The L-type calcium channel complex is composed of multiple subunits, but the alpha-1C subunit forms the channel's core, determines its biophysical properties, and binds most drugs. Dysfunction or genetic variants of this protein can play roles in some neurological and cardiac diseases[2][5][1].

Other names
CaV1.2CACNA1C (gene name)L-type calcium channel alpha-1C subunitL-type voltage-dependent calcium channel alpha-1 subunit
02

Mechanism of action

Blockade or inhibition of calcium influx by binding to the channel’s alpha-1 subunit, thereby reducing contractility and conduction in cardiac and smooth muscle. Modulation of action potential duration and amplitude in excitable tissues. Decreased aldosterone secretion by endocrine cells.

03

Biological functions

Mediates calcium ion influx in response to membrane depolarizationExcitation-contraction coupling in cardiac, smooth, and skeletal muscleRegulation of heart rhythmEndocrine secretion (e.g., aldosterone)Blood pressure control via smooth muscle contraction
04

Disease associations

Cardiovascular disease (e.g., hypertension, arrhythmias, angina, heart failure)Neuropsychiatric disorders (e.g., autism, bipolar disorder—via genetic variation, not drug action)Muscle disordersOther (e.g., some roles in endocrine diseases)
05

Safety considerations

HypotensionBradycardia or heart blockNegative inotropic effects (risk in heart failure or conduction defects)Peripheral edemaPotential exacerbation of heart failure with excessive inhibition
06

Interacting drugs

Dihydropyridines (e.g., amlodipine, nifedipine)

2 more in the full profile.

07

Biomarkers

Genetic variants (e.g., polymorphisms in CACNA1C)Expression levels of CACNA1C in tissues (rare in clinical use, mostly research)

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