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CACNA1C activates calcium(2+). 59 / 59
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"Studies in both systems revealed that expression of a transgene containing the Gly406Arg variant in exon 8A results in CACNA1C channels that have impaired VDI, leading to prolonged opening of the channel and subsequently increased Ca flux through the channel (4)."
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"We tested the hypothesis that the altered phosphorylation of Cav1.2 might underlie the sarcolemmal Ca 2+ influx phenotype in Cacna1c +/- myocytes using immunoblotting of the left ventricular (LV) tissue from Cacna1c +/- versus wildtype (WT) hearts."
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"The activation of Cav1.2 by plasma membrane depolarization allows Ca to flow into the cell; Ca binds to RyR2, a large homotetrameric Ca release channel expressed in cardiomyocytes and located on the SR membrane (Figure 1), and induces it to open and to release Ca from the SR, thus triggering muscle contraction."
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"Variants located in CACNA1C, CACNA1D, CACNA1F and CACNB2 cause gain of function by preventing voltage-dependent inactivation of Ca 1.2, Ca 1.3, Ca 1.4, and Ca β2, leading to excessive influx of Ca ."
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"The Cav1.2 mediates Ca influx into the cell and regulates a variety of cellular processes."
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"De La Mata et al. showed that the T-tubule associated protein BIN1 (Bridging integrator 1) expression promotes the formation of the extensive tubular distribution and suggested that its expression along the sarcolemma can promote clustering of Cav1.2, which increases the chance of cooperative gating and calcium influx involved in excitation contraction coupling."
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"The conformational change of Cav1.2 induces a Ca 2+ current that locally changes the concentration of Ca 2+ near the RyR2, stimulating Ca 2+ release through a process known as Ca 2+ -induced Ca 2+ -re[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Alternative splicing in CACNA1C, encoding the Ca V 1.2 pore forming subunit alpha1 C, modulates the function of Ca V 1.2 calcium channels."
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"Alternative splicing in CACNA1C, encoding the Ca V 1.2 pore forming subunit alpha1 C, modulates the function of Ca V 1.2 calcium channels."
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"Similarly, variability of the clinical symptoms due to genetic mosaicism has been discussed for Timothy syndrome caused by pathogenic CACNA1C (Ca 1.2) variants."
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"Cav1.2 primarily mediates Ca influx in ameloblastoma cells, as demonstrated by the use of agonists and blockers."
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"As the main intracellular Ca 2+ influx pathway, L -type calcium channel (Cav1.2) causes changes in transmembrane potential by controlling the entry of Ca 2+ into cells, and plays an important role in [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"CaV1.2, which is composed of the α1 subunit, β subunit and the α2δ subunit [16], mediates the inward L‐type calcium current (I ) and contributes to the plateau phase of the cardiac action potential due to enhanced membrane depolarization."
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"A model in which dorsal and ventral telencephalic organoids were fused was applied to investigate TS caused by mutations in the CACNA1C gene encoding the calcium voltage-gated channel subunit α1C."
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"The overexpression of β2a-subunit increases the open probability and membrane trafficking of the pore-forming Cav1.2α1c-subunit, which further increased Ca influx in cardiomyocytes as previously reported (21, 22)."
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"Cav1.2, mediating the inward L -type Ca 2+ current (I Ca-L ), is the predominant Ca 2+ channel type in cardiac myocytes."
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"The cardiac L-type calcium channel (Cav1.2) determines the action potential duration, initiates intracellular calcium transients and triggers heart contraction."
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"Ketamine inhibited Cav1.2 expressed in Xenopus oocytes, and similarly inhibited L-type Ca channel activity in freshly isolated mouse bladder smooth muscle cells."
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"In parallel, Cav1.2 has been found to be constitutively expressed by preosteoblasts and may mediate Ca influx in response to depolarization [37]."
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"Additionally, DMD EHTs displayed increased expression of genes related to excitation-contraction coupling and regulation of membrane potential (SCN5A, CACNA1G, CACNA1C), which could point toward membrane hyper-excitability and increased Na and Ca currents causing prolongation of action potentials and increased incidence of early after depolarizations."
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"CACNA1C, a calcium channel gene, mediates the entry of calcium ions into excitable cells and is also involved in a variety of calcium dependent processes, including muscle contraction, hormone and neurotransmitter release, gene expression, cell motility, cell division and cell death."
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"The calcium voltage-gated channel subunit alpha1 C (CACNA1C) in T-tubules induced the extracellular calcium influx into the cell (calcium sparks formation) by the depolarized cell membrane."
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"Expression of Cacna1c and Cacna2d2/Cacna2d3, encoding subunits of the L-type Ca channel, was upregulated in the atrium of Tbx5 mice."
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"Here, we report that deletion of Cacna1c in neurons of the developing brain disrupts spontaneous calcium activity and causes abnormal brain development and anxiety."
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"XREF_BIBR, XREF_BIBR, XREF_BIBR In particular, induced neurons from subjects with the risk CACNA1C single nucleotide polymorphism show greater expression of calcium channel subunit mRNA, and increased calcium signalling, compared to those without the risk allele."
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"Taken together, Cav1.2‐mediated intracellular Ca is essential for the AM‐1 or primary AM cell aggregation and collective migration.3.4 L-type VGCC-mediated Ca 2+ influx during AM spheroids collective invasion."
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"Our findings reveal that disruption of Cacna1c perturbs spontaneous Ca activity in neural progenitors, affecting cerebral cortical development and causing anxiety in adulthood."
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"The correlation between the relative amount of CACNA1C and the rate of pressure generation is logical as CACNA1C initiates the calcium current into the cytosol and causes the RyR-2 to release calcium from the sarcoplasmic reticulum into the cytosol, which finally leads to contraction."
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"miR-26a is expressed in β-cells and inhibits expression of voltage-gated L-type calcium channel subunit-α1C (CACNA1C), which mediates calcium influx and insulin granule fusion ."
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"Cacna1c Modulates Spontaneous Ca 2+ Activity in Brain Slices.."
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"Together, these data reveal that the disruption of Cacna1c perturbs spontaneous Ca activity in neocortical neural progenitors during development."
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"Intriguingly, Cacna1c appears to be up-regulated in the cortical intermediate zone to stimulate spontaneous Ca oscillations in neural progenitors and radial migration (62)."
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"CACNA1C, as a subunit of voltage-dependent calcium channel, may mediate calcium ions influx into the cell upon membrane polarization [22, 23]."
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"TCONS_00075467 was found to be down-regulated in the RA tissue of AF rabbit model and acted as a ceRNA for miR-328 to down-regulate the expression of CACNA1C and induce intracellular calcium overload."
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"CACNA1C modulates calcium influx, potentially disrupting rhythms."
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"In previous simulation studies, it has been shown that changes in I CaL due to gain-of-function mutations in CACNA1C prolongs action potential duration linked to early afterdepolarizations, and increases SR calcium content which is then responsible for spontaneous calcium release and delayed afterdepolarizations."
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"LQT8 and Timothy syndrome are caused by mutation in the CACNA1C gene encoding the L-type Ca 2+ channel."
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"PKA-mediated phosphorylation of Cav1.2 enhances the L-type Ca currents and also affects the channel inactivation properties [63]."
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"We did not confirm whether a CACNA1C variant, p.R412M, caused the same electrophysiological effects on Ca 1.2 when exon 8 expressed."
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"In rat smooth muscle cells alpha5beta1 integrin signalling has been described to promote CACNA1C mediated calcium entry in cells through Src phosphorylation of CACNA1C on Y2122."
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"APP-KO mice show increased levels of Cav1.2 and subsequent increase in GABAergic calcium currents."
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"Following the designation introduced by Tang, et al. [XREF_BIBR], we designed qPCR primers to assay three classes of splice variants previously shown to encode distinct CACNA1C isoforms that produce calcium channel subunits with different activation potentials."
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"In chronic heart diseases accompanied by cardiac arrhythmias, there is an increase in the activity of Cav1.2 channels, which leads to an increase in their permeability to Ca and, as a result, to CM calcium overload."
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"Palmitoylation of Cav1.2 can enhance its anchoring to the membrane [156], stabilizing its function and allowing more efficient calcium entry into cells."
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"Specifically, mutations in the CACNA1C gene cause an abnormal function of this calcium channel, and have been associated with BP, SCZ and another syndromic form of ASD, Timothy syndrome (TS)."
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"Increased CACNA1C expression leads to dysregulated Ca signaling and an elevated risk of psychiatric disorders."
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"CACNA1C forms an ion channel pore to allow calcium ions to enter the cytosol, which is essential for cellular calcium signaling, neuronal excitability, muscle contraction, and regulation of gene expression (Bozarth et al. 2018)."
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"Whole-cell patch clamping revealed the effect of CRMP4 SUMOylation on Cav1.2 mediated calcium influx."
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"Longer exposure to METH (20 min or 48 hr) selectively upregulates the expression of only the CACNA1C gene, thus increasing the number of L-type Ca 2+ channels."
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"Many of these risk genes encode proteins involved in calcium signaling including CACNA1C, CACNB2, and CACNA1I that may ultimately converge on a common disease mechanism XREF_BIBR, XREF_BIBR."
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"Conditional knockdown of Cav1.2 in astrocytes can block calcium influx by 80% and reduce LPS-induced activation and proliferation of astrocytes [60]."
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"Timothy syndrome (TS) is an autosomal dominant disorder, and is caused by a mutation in the cacna1c gene encoding the calcium channel Ca v 1.2 subunit."
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"Cav1.2 and Cav1.3 in the L-type voltage-gated Ca channels are associated with PD [27] and Cav1.2 is prevalent in juvenile SNc (Substantia Nigra) DA neurons, but in senescent SNc DA neurons, Cav1.3 is preferentially used for Ca inflow, allowing Ca to enter through an oscillatory pathway that contributes to the membrane potential threshold, which is the basis of autonomous pacing [28]."
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"Timothy syndrome (TS) is an autosomal dominant disorder, and is caused by a mutation in the cacna1c gene encoding the calcium channel Ca v 1.2 subunit."
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"This gene encodes an alpha-1 subunit of the voltage-gated L-type calcium channel (Cav1.2), which mediates the influx of calcium ions into the cell upon membrane polarization and plays a role in dendritic development, neuronal survival, synaptic plasticity, and memory/learning (36)."
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"Cell lines derived from BP patients in this study harbor a single nucleotide polymorphism, rs1006737, in the L-type calcium channel gene CACNA1C, which mediates calcium influx into the cell and has been associated with BP as well as with schizophrenia."
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"In the heart, Ca binding to resident CaM on Cav1.2 mediates Ca -dependent inactivation (CDI) of inward L-type Ca current which is important for controlling cardiac action potential duration (APD)."
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"The knockdown of Cacna1c also reduces the glutamate-induced increase of mitochondrial ROS production, intramitochondrial calcium influx and cell death in HT22 cells [180]."
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"Mutations in CACNA1C cause a significant increase in the sustained intracellular calcium rise, leading to changes in gene expression and altered neuronal differentiation, partly through changes in early growth response protein (Egr1) transcription factor levels [XREF_BIBR]."
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