CACNA1D

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CACNA1D

A gene on chromosome 3p14.3 that encodes the alpha-1D subunit of a voltage-dependent L-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. CACNA1D gives rise to L-type calcium channels which belong to the high-voltage activated (HVA) group.
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Downregulation of Cav1.3 calcium channel expression in the cochlea is associated with age-related hearing loss in C57BL/6J mice.
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.
From automatic plotting of dissolution and amplification curves in ABI 7500 and base sequence results of Invitrogen, Cav1.2, Cav1.3, three subtypes of IP[sub]3 Rs, RyR2, iNOS, and nNOS were positive in the achalasia and control groups (esophageal circular muscle, EC), but other subtypes were negative [Figure 1]a.
Expression of Cav1.3, CaMKII, and p-CaMKII (Thr286) in the striatum was detected using Western blot analysis.
Treadmill Exercise Decreases the Expression of Cav1.3 and p-CaMKII (Thr286) in the Striatum of PD Rats.
A ello se agregan isoformas predominantes de los canales de calcio conocidos como canales de calcio tipo L (CCTL) denominados Cav1.2 y Cav1.3, que se encuentran en el sistema nervioso central que muestran una expresion generalizada en varias regiones del cerebro, tales como la corteza cerebral, la amigdala, el cerebelo y el hipocampo, por lo que se ha reconocido que las corrientes de Ca2 + tipo L regulan la excitabilidad neuronal, la plasticidad sinaptica, y la transcripcion de genes a nivel neuronal, asi como la transcripcion de genes asociados con los cambios a largo plazo en la plasticidad sinaptica, la proliferacion celular, la muerte celular programada.
(2014) The role of L-type voltage-gated calcium channels Cav1.2 and Cav1.3 in normal and pathological brain function.
Mechanistically, S[O.sub.2] and its derivatives induced the [K.sub.ATP] and B[K.sub.Ca] channels activation through increasing the expressions of Kir6.1, Kir6.2, SUR2B, and B[K.sub.Ca] channel subunits [alpha] and [beta]1 in rat aortic rings, while S[O.sub.2] and its derivatives inhibited the L-type calcium channel through decreasing the expressions of Cav1.2 and Cav1.3 [30].
Loss of Cav1.3 (CACNA1D) function in a human channelopathy with bradycardia and congenital deafness.
Functional interaction of neuronal Cav1.3 L-type calcium channel with ryanodine receptor type 2 in the rat hippocampus.
Direct interaction of otoferlin with syntaxin 1A, SNAP-25, and the L-type voltage-gated calcium channel Cav1.3. J Biol Chem.
If the concentration of SO[sub]2 is >500 [micro]mol/l, the vasodilatory effects are independent of the endothelial system but related to K[sub]ATP channels and the inhibition of L-type calcium channels.[22],[23],[24] In contrast, if the concentration of SO[sub]2 is <450 [micro]mol/L, the vasorelaxant mechanism depends on the big-conductance calcium-activated K + (BKCa) and cyclic guanosine monophosphate.[24] SO[sub]2 induced the K[sub]ATP and BKCa channel activation via upregulating the expressions of Kir6.1, Kir6.2, SUR2B, and BKCa channel subunits a and [sz]1 in rat aortic rings, while SO[sub]2 inhibited the L-type calcium channel by downregulating the Cav1.2 and Cav1.3 expressions.[25]