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Mammalian Monoclonal CACNA1C Primary Antibody for ISt, IHC - ABIN1304574
Li, Li, Chen, Chen, Hu, Pan: Potentiation of high voltage-activated calcium channels by 4-aminopyridine depends on subunit composition. in Molecular pharmacology 2014
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Mammalian Monoclonal CACNA1C Primary Antibody for ISt, IHC - ABIN1304575
Perissinotti, Ethington, Almazan, Martínez-Hernández, Kalil, Koob, Piedras-Rentería: Calcium current homeostasis and synaptic deficits in hippocampal neurons from Kelch-like 1 knockout mice. in Frontiers in cellular neuroscience 2015
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Mouse (Murine) Monoclonal CACNA1C Primary Antibody for Func, FACS - ABIN2191860
Shibata, Berney, Reininger, Chicheportiche, Ozaki, Shirai, Izui: Monoclonal anti-erythrocyte autoantibodies derived from NZB mice cause autoimmune hemolytic anemia by two distinct pathogenic mechanisms. in International immunology 1991
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Human Polyclonal CACNA1C Primary Antibody for WB - ABIN550312
Green, Warre, Hayes, McNaughton, Medhurst, Pangalos, Duckworth, Randall: Kinetic modification of the alpha(1I) subunit-mediated T-type Ca(2+) channel by a human neuronal Ca(2+) channel gamma subunit. in The Journal of physiology 2001
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Human Monoclonal CACNA1C Primary Antibody for ICC, IF - ABIN447361
Carnevale, Vecchione, Mascio, Esposito, Cifelli, Martinello, Landolfi, Selvetella, Grieco, Damato, Franco, Haase, Maffei, Ciraolo, Fucile, Frati, Mazzoni, Hirsch, Lembo: PI3Kγ inhibition reduces blood pressure by a vasorelaxant Akt/L-type calcium channel mechanism. in Cardiovascular research 2011
Polyclonal CACNA1C Primary Antibody for ELISA, WB - ABIN539744
Saud, Minobe, Wang, Han, Horiuchi, Hao, Kameyama: Calpastatin binds to a calmodulin-binding site of cardiac Cav1.2 Ca2+ channels. in Biochemical and biophysical research communications 2007
CACNA1C CpG-SNPs are associated with PTSD in traumatized police officers.
Study presents evidence that CaV1.2 moves in vesicular structures of circular and tubular shape with diverse intracellular and submembrane trafficking patterns. Both microtubules and actin filaments are required for dynamic movement of CaV1.2 vesicles. These vesicles undergo constitutive homotypic fusion and fission events that sustain CaV1.2 clustering, channel activity and cooperative gating.
CACNA1C polymorphism and childhood interpersonal trauma were related to brain activation for group and emotion specific processing.
Case-control study suggested that rs10848683 in CACAN1C increased the susceptibility to large-artery atherosclerotic (LAA) stroke, the CC genotype of rs10848683 maybe a risk factor for LAA stroke under the recessive models. The haplotypes of rs229961-rs215976-rs216008-rs10848683 in CACAN1C also showed increased risk of LAA stroke.
miR-137 regulated the expression of the CACNA1C gene.
This is the first study to suggest the involvement of the novel missense CACNA1C c.1786G>A and TTN c.49415G>A variants in the inheritance of symptomatic bradycardia and development of sick sinus syndrome.
MYH7-V878A and CACNA1C-A1594V mutations were detected in a Chinese Family with Hypertrophic Cardiomyopathy. Those with only the CACNA1C-A1594V mutation showed nearly normal readings in all examinations. The results suggest that the pathogenesis of MYH7-V878A and CACNA1C-A1594V mutations may have a cumulative effect.
Study established cognitive effects of risk variants at loci implicated in synaptic transmission by (1) identifying GWAS schizophrenia variants whose associated gene function is related to synaptic transmission, and (2) testing for association between these and measures of neurocognitive function; suggest that CACNA1C risk variant rs2007044 is associated with poorer memory function and cortical dysconnectivity.
Increased repolarization dispersion caused by the G1911R mutation is a primary factor that may primarily contribute to the genesis of cardiac arrhythmias in Timothy Syndrome.
Data indicate that a cardiac protein named Myoscape/FAM40B/STRIP2, which directly interacts with the L-type calcium channel CaV1.2.
The results show that estrogen upregulates cardiac L-type Ca(2+) and sodium-calcium exchange in women through genomic mechanisms that account for sex differences in Ca(2+) handling and spatial heterogeneities of repolarization due to base-apex heterogeneities of Cav1.2alpha and NCX1. By analogy with rabbit studies, these effects account for human sex-difference in arrhythmia risk.
Study reveal a significant association of CACNA1C with bipolar disorder among the Pakistani population, extending results from other ethnic groups to the Pakistani population for the first time.
This study demonstrated that CACNA1C gene polymorphisms and CACNA1C protein expression were associated with schizophrenia and its clinical phenotypes.
We suggest the possibility that our findings of differential brain activations and methylation status of the CACNA1C gene in suicidal attempt patients might be involved in the neurobiology of suicidal behavior.
The main findings of this study are that (1) CACNA1C gene polymorphism (rs10774053) can increase ritodrine-induced ADEs; (2) maximum infusion rate of ritodrine was significantly associated with ADE occurrence.
The results of this study increasing the risk for Bipolar Disorder in the presence of the rs758723 T allele within CACNA1C.
Inhibition of CaV1.2 upregulates AT1R signaling in response to angiotensin II.
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, whereas among A non-carriers there was not an effect of age on left cACC cortical thinning.
The frequency of CACNA1C rs10848683 in genetic high-risk individuals was double that in controls. For SYNE1 rs214950, higher frequencies were found in the genetic high-risk group than in controls. Polymorphisms in CACNA1C and SYNE1 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.
The Shank3/F model, and to a much lesser extent, the Shank3/J and Cacna1c models, showed hypoactivity and a general anxiety-like behavior triggered by external stimuli which pervaded social interactions.
Proteolytic cleavage and phosphorylation of alpha1C subunit are not required for adrenergic regulation of CaV1.2 in the heart.
The data of this study illustrated an important role of CaV1.2 in fear extinction and the synaptic regulation of activity within the amygdala.
Cav1.2 mutation associated with Timothy syndrome has pleiotropic effects on the ascending serotonin system.
Cardiac specific expression of the mutated Cav1.2PKA_P2(-/-) gene reduces Cav1.2 alpha1c protein concentration, calcium current (ICa), and the beta-adrenergic stimulation of L-type ICa in cardiomyocytes.
the significant decrease or absence of exon 33-containing CaV1.2 channels is potentially proarrhythmic in the heart.
Findings suggest that REDD1 in cacna1c heterozygous mice may influence depression-related behavior via regulation of the FoxO3a pathway. Study identified the prefrontal cortex as a key brain region in which cacna1c mechanisms through previously unidentified, novel molecular pathways contribute to depression-related behavior.
Normal regulation of CaV1.2 channels by phosphorylation of Ser1700 in cardiomyocytes is required for cardiovascular homeostasis and normal physiological regulation in vivo.
Cacna1c reduction causally predisposes to the maladaptive outcomes of social stress.
Deletion of psychiatric risk gene Cacna1c impairs hippocampal neurogenesis
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.
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.
S1928A KI mice failed to induce long-term potentiation in response to prolonged theta-tetanus (PTT-LTP), a form of synaptic plasticity that requires Cav1.2 and enhancement of its activity by the beta2-adrenergic receptor (beta2AR)-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-positive adult-born neurons.
The present study shows that ANO1 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.
CaV1.2 expression is tightly regulated through Wnt signaling and plays an essential sensory role in primary cilia necessary for cellular homeostasis
findings suggested that the expressions of the cardiac CACNA1C were under the CLOCK-BMAL1 regulation, probably through the PI3K-Akt 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+)-dependent regulation of Cav1.2
Competitive and non-competitive regulation of calcium-dependent inactivation in CaV1.2 L-type Ca2+ channels by calmodulin and Ca2+-binding protein 1.
(CaV1.2 alpha-1) Cav1.2 alpha-1 binds specifically to CaMKII in forebrain to enhance regulatory phosphorylation.
a model where high affinity binding of Ca(V)beta to the I-II linker of Ca(V)alpha1 largely accounts for Ca(V)beta-induced plasma membrane targeting of Ca(V)1.2
The identification of seven PKC phosphorylation sites within the alpha(1c) subunit, is reported.
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 structural analysis and comparison to CaV1.2 channel
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.
DHPR, alpha-1 subunit
, calcium channel, L type, alpha-1 polypeptide, isoform 1, cardiac muscle
, calcium channel, cardic dihydropyridine-sensitive, alpha-1 subunit
, voltage-dependent L-type calcium channel subunit alpha-1C
, 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
, island beat
, L-type voltage-gated calcium channel alpha1C subunit ChCaChA1C
, L-type Ca channel alpha 1 subunit
, L-type calcium channel CaV1.2
, atrium L-type calcium channel
, L-type voltage-dependent calcium channel alpha-1 subunit
, 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
, voltage-gated calcium channel alpha 1C subunit
, breakpoint cluster region protein