CACNA1C

(redirected from Cav1.2)
Also found in: Wikipedia.

CACNA1C

A gene on chromosome 12p13.3 that encodes the alpha-1C subunit of a voltage-dependent N-type calcium channel, which mediates the entry of calcium ions into excitable cells. These channels are also involved in various calcium-dependent processes, including muscle contraction, hormone or neurotransmitter release, gene expression, cell motility, cell division and apoptosis. CACNA1C is the pore-forming subunit of an N-type voltage-dependent calcium channel, which controls neurotransmitter release from neurons.

Molecular pathology
Defects of CACNA1C cause Timothy syndrome and Brugada syndrome type 3.
References in periodicals archive ?
Evidence suggests that (3-11) chemerin may influence cardiovascular functions and the expressions of PI3K alpha (PI3K[alpha]), PI3K gamma (PI3K[gamma]), beta adrenergic receptor 1 ([beta]1-AR), [beta]2-AR, endothelial nitric oxide synthase (eNOS), sarcolemmal L-type [Ca.sup.2+] channel (CaV1.2) genes, and the tissue levels of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP).
IHC and scoring were conducted as described.[9] Primary antibodies of inducible NOS (iNOS) (mouse, Abcam, ab129372), neuronal NOS (nNOS) (rabbit, Abcam, ab3511), Cav1.2 (mouse, Abcam, ab84814), Cav1.3 (mouse, Abcam, ab85491), IP[sub]3R1 (rabbit, Abcam, ab125076), IP[sub]3R2 (rabbit, Millipore, ab9074), IP[sub]3R3 (rabbit, Millipore, ab9076), and RyR2 (rabbit, Chemicon, ab9080) were diluted at 1:100.
Although inhibition of the hERG channel (human ether-a-go-go-related gene) regulating the major repolarizing current in the heart, IKr (delayed inward potassium current), is the most common mechanism of QT prolongation [4, 5], it can also be caused by the drug triggered inhibition of other channels, that is, potassium (Kv7.1), sodium (Nav1.5), or calcium (Cav1.2) [6-9].
Yang et al., "Splice variant specific modulation of CaV1.2 calcium channel by galectin-1 regulates arterial constriction," Circulation Research, vol.
Most recent studies have investigated L-type (CaV1.2) and T-type (CaV3.1) VGCCs in adult cultured NSCs and have detected their expression at the transcriptional or translational levels [37].
Palade, "Angiotensin II upregulates CaV1.2 protein expression in cultured arteries via endothelial [H.sub.2][O.sub.2] production," Journal of Vascular Research, vol.
However, the expression of L-type calcium channel alpha 1C subunit (Cav1.2) was similar between groups (Figures 4(d) and 4(e)).
Welling et al., "Dominant role of smooth muscle L-type calcium channel Cav1.2 for blood pressure regulation," The EMBO Journal, vol.
Homer1 activity has been shown to influence the functioning of other proteins and protein complexes linked to psychiatric disorders through genetic variants, such as FMRP [28, 42, 43], CYFIP1 [27, 44, 45], Arc [27, 46], SHANK [10, 47, 48], and the calcium channel Cav1.2 [16, 42].
Spatial association of the Cav1.2 calcium channel with [alpha]5[beta]1-integrin.
On the other hand, conduction through the SAN and AV node is partially determined by [Ca.sup.2+] influx specifically via Cav1.2 channels, whose pore domain patency determines the L-type [Ca.sup.2+] current (Maltsev and Lakatta 2008).