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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)
Carriers of the CACNA1C allele A exhibited greater left mOFC thickness compared to non-carriers. Moreover, CACNA1C A carriers showed age-related cortical thinning of the left cACC (show CLCA1 ELISA Kits), whereas among A non-carriers there was not an effect of age on left cACC (show CLCA1 ELISA Kits) cortical thinning.
The frequency of CACNA1C rs10848683 in genetic high-risk individuals was double that in controls. For SYNE1 (show SYNE1 ELISA Kits) rs214950, higher frequencies were found in the genetic high-risk group than in controls. Polymorphisms in CACNA1C and SYNE1 (show SYNE1 ELISA Kits) could confer a greater risk of developing Schizophrenia and Bipolar Disorder in individuals who are already at high risk because of their family history.
Top association findings suggested that the bipolar disorder risk allele at SNP rs4765913 in CACNA1C gene may be associated with increased risk of cardiac dysrhythmias.
Data indicate a subpopulation of the CaV1.2 channel pore-forming subunit (alpha1C) within nanometer proximity of protein kinase A (PKA) at the sarcolemma of murine and human arterial myocytes.
Targeted sequencing revealed trigenic mutations: c.700G>A/p.E234K in DES (show DES ELISA Kits), c.2966G>A/p.R989H in MYPN (show MYPN ELISA Kits), and c.5918G>C/p.R1973P in CACNA1C in a family of hypertrophic cardiomyopathy with early repolarization and short QT syndrome.
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.
A novel and selective role was found for the Cav1.2 channel in the hippocampus that mediates extinction of cocaine conditioned place preference.
Findings indicate tissue-specific differences in L-type calcium channel CaV1.2 regulation and suggest that it may be possible to design therapies to target this channel in specific tissues.
S1928A KI mice failed to induce long-term potentiation in response to prolonged theta-tetanus (PTT-LTP (show SCP2 ELISA Kits)), a form of synaptic plasticity that requires Cav1.2 and enhancement of its activity by the beta2-adrenergic receptor (show ADRB2 ELISA Kits) (beta2AR (show ADRB2 ELISA Kits))-cAMP-PKA cascade.
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.
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 interaction with the channel.
CaM may tether to the channel with its single lobe, leading to multiple CaM 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