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Mammalian Monoclonal CACNA1C Primary Antibody für 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 für 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 für 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 für ELISA, WB - ABIN449706
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
Human Monoclonal CACNA1C Primary Antibody für 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
This is the first study to suggest the involvement of the novel missense CACNA1C c.1786G>A and TTN (zeige TTN Antikörper) c.49415G>A variants in the inheritance of symptomatic bradycardia and development of sick sinus syndrome.
MYH7 (zeige MYH7 Antikörper)-V878A and CACNA1C-A1594V mutations were detected in a Chinese Family with Hypertrophic Cardiomyopathy. Those with only the CACNA1C-A1594V mutation showed nearly normal (zeige EEF1G Antikörper) readings in all examinations. The results suggest that the pathogenesis of MYH7 (zeige MYH7 Antikörper)-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.
Data indicate that a cardiac protein named Myoscape/FAM40B/STRIP2 (zeige STRIP2 Antikörper), which directly interacts with the L-type calcium channel CaV1.2.
The results show that estrogen upregulates cardiac L-type Ca(2 (zeige CA2 Antikörper)+) and sodium-calcium exchange in women through genomic mechanisms that account for sex differences in Ca(2 (zeige CA2 Antikörper)+) handling and spatial heterogeneities of repolarization due to base-apex (zeige APEX1 Antikörper) heterogeneities of Cav1.2alpha and NCX1 (zeige SLC8A1 Antikörper). 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.
ox-LDL, as a known factor in atrial fibrillation-associated remodeling, positively regulates miRNA-223 transcription and L-type calcium channel CACNA1c protein expression
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 Shank3 (zeige SHANK3 Antikörper)/F model, and to a much lesser extent, the Shank3 (zeige SHANK3 Antikörper)/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 (zeige DDIT4 Antikörper) in cacna1c heterozygous mice may influence depression-related behavior via regulation of the FoxO3a (zeige FOXO3 Antikörper) 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
CaV1.2 expression is tightly regulated through Wnt (zeige WNT2 Antikörper) 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 (zeige ARNTL Antikörper) regulation, probably through the PI3K-Akt (zeige AKT1 Antikörper) 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 (zeige CA2 Antikörper)+)-dependent regulation of Cav1.2
Competitive and non-competitive regulation of calcium-dependent inactivation in CaV1.2 L-type Ca2 (zeige CA2 Antikörper)+ channels by calmodulin and Ca2 (zeige CA2 Antikörper)+-binding protein 1.
(CaV1.2 alpha-1) Cav1.2 alpha-1 binds specifically to CaMKII (zeige CAMK2G Antikörper) 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 (zeige CACNA1G Antikörper) 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