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Competitive and non-competitive regulation of calcium-dependent inactivation in CaV1.2 L-type Ca2 (show CA2 ELISA Kits)+ channels by calmodulin and Ca2 (show CA2 ELISA Kits)+-binding protein 1.
Surface biotinylation and flow cytometry assays revealed that L-type calcium channel alpha(1C) channels composed of the corresponding alpha-actinin (show ACTN1 ELISA Kits)-binding-deficient mutants result in a 35-40% reduction in surface expression compared to that of wild-type channels.
a direct physical interaction between the N terminus (NT) and C terminus (CT) of the main subunit of the L-type Ca(2 (show CA2 ELISA Kits)+) channel CaV1.2, alpha1C, is reported.
These results reveal a new dimension of regulation of Ca(V)1.2 channels through phosphorylation of the Hook domains of their beta subunits.
These findings suggest that N-glycosylation contributes to the surface expression and voltage-dependent gating of Cav1.2.
Data show that cardiac L-type calcium (CaV1.2) channels form clusters that undergo dynamic, reciprocal, allosteric interactions.
these findings provide evidence for a new role of Homer1 (show HOMER1 ELISA Kits) supporting the regulation of Cav1.2 channels by STIM1 (show STIM1 ELISA Kits).
structural flexibility of CaV1.2 and CaV2.2 (show CACNA1B ELISA Kits) I-II proximal linker
These results suggest a complex antagonistic interplay between G(q)-activated PKC and Gbetagamma in regulation of L-VDCC, in which multiple cytosolic segments of alpha(1C) are involved.
There were substantial transmural gradients in Cav1.2, KChIP2 (show KCNIP2 ELISA Kits), ERG (show KCNH2 ELISA Kits), KvLQT1 (show KCNQ1 ELISA Kits), Kir2.1 (show KCNJ2 ELISA Kits), NCX1 (show SLC8A1 ELISA Kits), SERCA2a (show ATP2A2 ELISA Kits) and RyR2 (show RYR2 ELISA Kits) at the mRNA and, in some cases, protein level-in every case the mRNA or protein was more abundant in the epicardium than the endocardium.
Ca v1.2 binding site for PP2A and PP2B (show CAN ELISA Kits)
We report the case of female child with a history of surgery for syndactyly of the hands and feet, Despite the absence of facial dysmorphism and the presence of normal psychomotor development, a diagnosis of Timothy syndrome was made given association of syndactyly and the ECG features. Sanger sequencing of the CACNA1C gene, followed by sequencing of the genes KCNQ1 (show KCNQ1 ELISA Kits), KCNH2 (show KCNH2 ELISA Kits), KCNE1 (show KCNE1 ELISA Kits), KCNE2 (show KCNE2 ELISA Kits), were negative.
CACNA1C variants for psychiatric disorders were found to be associated with long sleep latency among 8-month-old infants.
In type 2 diabtes beta cells, exocytosis was slower and not synchronized with membrane depolarizations, and neither Ca2 (show CA2 ELISA Kits)+ influx nor CaV1.2 was concentrated at insulin (show INS ELISA Kits) granules.
the loss-of-function CACNA1C-Q1916R mutation contributed to Early repolarization syndrome-related sudden cardiac death.
BIMU8 is a potent blocker of hERG (show KCNH2 ELISA Kits), NaV1.5 (show SCN5A ELISA Kits) and CaV1.2 cardiac ion channels, inducing cardiac arrhythmias.
CACNA1C rs1006737 SNP and SNPs in linkage disequilibrium with it may influence the risk of QTc prolongation in patients treated with psychotropic drugs with cardiovascular risk
Functional Characterization of Schizophrenia-Associated Variation in CACNA1C
Authors assessed the effect across the human brain of the CACNA1C rs1006737 genotype on FA, in a Caucasian clinical sample as well as in health, and whether this genotype effect was different between diagnostic groups and whether it interacted with the ZNF804A rs1344706 genotype.
The study supports the association of SNP rs1006737 with bipolar disorder-I (BD-I) and suggests that CACNA1C SNP rs1006737 and Bcl-2 SNP rs956572, or specific causal variants in linkage disequilibrium with these proxies, act independently to increase risk and Intracellular Ca(2+) dyshomeostasis (ICDH) in BD-I.
The Ca channel alpha 1C (CACNA1C) mRNA and protein expressions were noticeably elevated in H-Cd group. These findings suggest that CACNA1C might be implicated in Cd transport in human placenta.
Cav1.2 can modulate oligodendrocyte maturation in the demyelinated brain and is critical for remyelination.
CaV1.2 knock-out mice exhibited normal acquisition and recall of the location of the hidden platform in a standard Morris water maze, but were unable to form a memory of when the number of available spatial cues was restricted. Within the dentate gyrus, pan-neuronal deletion of CaV1.2 resulted in decreased cell proliferation and the numbers of doublecortin (show DCX ELISA Kits)-positive adult-born neurons.
The present study shows that ANO1 (show ANO1 ELISA Kits) and CavL play a central role in the generation of slow waves, phasic contractions and tone in the internal anal sphincter and that this pathway can occur in the absence of stretch
Cacna1c haploinsufficient mice lack normal sensitivity to inhibition of the dopamine transporter. Cacna1c is crucial for normal behavioral responses to DA stimulants.
Data (including data from studies using transgenic/knockout mice) suggest Cacna1c is involved in specific aspects of learning (behavioral strategies for increasing reward rate); majority of Cacna1c knockout mice manage to increase reward feedback across trials but appear to do so by adapting outcome-based behavioral strategy, while majority of control mice appear to adopt experimentally intended cue-association behavior.
This study showed that Cav1.2, but not Cav1.3 (show CACNA1D ELISA Kits), L-type calcium channel subtype mediates nicotine-induced conditioned place preference in mice.
We report that the protein densin-180 (show LRRC7 ELISA Kits) is highly enriched at excitatory synapses in the brain and enhances the cell surface trafficking and postsynaptic localization of Cav1.2 L-type Ca(2 (show CA2 ELISA Kits)+) channels in neurons. This interaction promotes coupling of Cav1.2 channels to activity-dependent gene transcription.
These results indicate that Cav1.2 modulates oligodendrocyte development and suggest that Ca(2 (show CA2 ELISA Kits)+) influx mediated by L-type voltage-operated Ca(2 (show CA2 ELISA Kits)+) channels inoligodendrocyte progenitor cells is necessary for normal myelination
The authors show that phosphorylation of S1928 displaces the beta-2 adrenergic receptor (show ADRB2 ELISA Kits) from Cav1.2 upon beta-adrenergic stimulation rendering Cav1.2 refractory for several minutes from further beta-adrenergic stimulation.
findings suggest that Hap1 (show HAP1 ELISA Kits) is important for insulin (show INS ELISA Kits) secretion of pancreatic beta-cells via regulating the intracellular trafficking and plasma membrane localization of Cav1.2, providing new insight into the mechanisms that regulate insulin (show INS ELISA Kits) release from pancreatic beta-cells.
These results suggest that structural rearrangements of CaV1.2 generated through the binding of BayK8644 or FPL64176, by altering the channel activity, could affect depolarization-evoked catecholamine secretion prior to cation transport.
CaV3.1 (show CACNA1G ELISA Kits) structural analysis and comparison to CaV1.2 channel
findings suggested that the expressions of the cardiac CACNA1C were under the CLOCK-BMAL1 (show ARNTL ELISA Kits) regulation, probably through the PI3K-Akt (show AKT1 ELISA Kits) signal pathway
These results suggest that PKA and phosphatase(s) attached on or near the Ca(V)1.2 channel regulate the basal channel activity, presumably through modulation of the dynamic CaM (show CALM PLURAL_@27096@) interaction with the channel.
CaM (show CALM ELISA Kits) may tether to the channel with its single lobe, leading to multiple CaM (show CALM ELISA Kits) molecule binding to increase the grade of Ca(2 (show CA2 ELISA Kits)+)-dependent regulation of Cav1.2
This gene encodes an alpha-1 subunit of a voltage-dependent calcium channel. Calcium channels mediate the influx of calcium ions into the cell upon membrane polarization. The alpha-1 subunit consists of 24 transmembrane segments and forms the pore through which ions pass into the cell. The calcium channel consists of a complex of alpha-1, alpha-2/delta, beta, and gamma subunits in a 1:1:1:1 ratio. There are multiple isoforms of each of these proteins, either encoded by different genes or the result of alternative splicing of transcripts. The protein encoded by this gene binds to and is inhibited by dihydropyridine. Alternative splicing results in many transcript variants encoding different proteins. Some of the predicted proteins may not produce functional ion channel subunits.
, island beat
, voltage-dependent L-type calcium channel subunit alpha-1C
, L-type Ca channel alpha 1 subunit
, L-type calcium channel CaV1.2
, atrium L-type calcium channel
, calcium channel, voltage-dependent, L type, alpha 1C subunit
, voltage-dependent L-type calcium channel subunit alpha-1C-like
, calcium channel voltage-dependent L type Cav1.2, alpha 1c subunit
, CaCB receptor
, smooth muscle calcium channel blocker
, DHPR, alpha-1 subunit
, calcium channel, L type, alpha-1 polypeptide, isoform 1, cardiac muscle
, calcium channel, cardic dihydropyridine-sensitive, alpha-1 subunit
, voltage-gated L-type calcium channel Cav1.2 alpha 1 subunit, splice variant 10*
, L-type Cav1.2
, brain class C
, calcium channel voltage-dependent alpha1c subunit
, neuronal voltage-gated calcium channel alpha 1C subunit
, skeletal muscle-specific calcium channel
, voltage-gated calcium channel subunit alpha Cav1.2
, L-type calcium channel alpha-1 subunit
, calcium channel, voltage-dependent, alpha 1C subunit
, voltage-gated calcium channel alpha 1C subunit
, L-type voltage-gated calcium channel alpha1C subunit ChCaChA1C
, L-type voltage-dependent calcium channel alpha-1 subunit
, cardiac L-type calcium channel
, Voltage-dependent L-type calcium channel subunit alpha-1C