IndraLab

Statements



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"Nfat5 knockdown suppresses Cacna1c expression, decreases L-type calcium current, and results in non beating ventricle."

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"LQTS‐associated CaM variants have been shown to perturb a range of other cardiac ion channels, including reducing the Ca ‐dependent inactivation of Cav1.2 (Gomez‐Hurtado et al., 2016; Limpitikul et al., 2014; Prakash et al., 2023; Yin et al., 2014), altered inhibition of RyR2 (Nomikos et al., 2014; Vassilakopoulou et al., 2015) and activation of CaMKIIδ (Berchtold et al., 2016; Prakash et al., 2023)."

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"In summary, the combined effects of the CACNA1C variant to diminish voltage dependent inactivation of Ca V 1.2 and increase window current expand our appreciation of mechanisms by which a gain of function of Ca V 1.2 can contribute to QT prolongation."

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"The Dolmetsch lab studied induced neurons from patients with Timothy Syndrome (TS), an extremely rare disorder associated with autism and cardiac abnormalities due to a mutation in the CACNA1C gene causing decreased inactivation of an L-type calcium channel subunit."

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"Because the CACNA1C risk allele is expected to produce loss of calcium channel function, we would expect BD patients without the risk allele to preferentially respond to CCB treatment."

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"Correspondingly, patch-clamp recordings revealed that increased expression of Cacna1c exon 8a reduced the sensitivity of Ca 1.2 channels to dihydropyridine blockade, attenuating vasodilation in small arteries.28 Although exons 21 and 22 of CACNA1C are mutually exclusive exons, there is an isoform that includes both exons."

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"Two further conserved NMP genes, CACNA1C [a calcium-channel auxiliary subunit/CaV1.2 implicated in maintaining calcium-channel inactivation (Soldatov et al., 1997)] and ATP2A1 [a calcium transporting ATPase that maintains low cytoplasmic calcium (Shull et al., 2003)], may additionally operate via different mechanisms to restrict intracellular calcium."

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"Briefly, Ca V 1.2- and Ca V 1.3-siRNA decreased Ca V 1.2 and Ca V 1.3 mRNA, respectively without affecting the gene expression of the other channel."

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"Conversely, CACNA1C p.A36V, which has a gain‐of‐function effect on VGCC and impairs neuronal Ca homeostasis, 8 was identified in patient 2, along with autistic traits."

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"Recent evidence has contributed to understand that inflammation signalling negatively interacts with the Ca -handling machinery in a mice model of inflammatory atrial cardiomyopathy, by downregulating Cacna1c, Ca -calmodulin-dependent protein kinase II (Camk2), Ryr2, and Serca2."

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"Here we present evidence that ketamine is an effective L-type Ca 2+ channel (Cav1.2) antagonist that directly inhibits calcium influx and smooth muscle contractility, leading to voiding dysfunction."

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"Increased CACNA1C expression leads to dysregulated Ca signaling and an elevated risk of psychiatric disorders."

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"As illustrated in XREF_FIG, expressions of SERCA2 (at gene and protein levels) and Cacna1c (at gene level) decreased in the hearts of 16-week high fat diet fed animals, suggesting altered myocardial Ca 2+ handling."

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"The consecutive downregulation of these two proteins leads to a decrease in the number and activity of CaV1.2 channels, which has been associated again with decreased cardiac excitability and decreased calcium influx, resulting in impaired contractile force and arrhythmias [73]."

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"The BD-RPEs were able to replicate multiple pathophysiological features of BD, including bestrophin-1 deficiency, downregulation of CACNA1C expression that disrupted intracellular calcium homeostasis, loss of the tight junction protein ZO-1, and reduction in the RPE’s phagocytic ability.Pomares et al. reported that mRNA expression level of BEST1 gene not only reflects disease progression but also disease severity ."

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"These data conclusively identify ketamine as a Cav1.2 antagonist which can block BSM cell Ca influx and inhibit BSM contractility."

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"The decreased expression of CACNA1C could induce intracellular calcium overload, which is the main mechanism of initiation and maintenance of AF."

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"A confidence interval of ≥ 95% was considered as significant.Previously, we have demonstrated that inactivation of the CACNA1C gene in hippocampal pyramidal cells virtually abolished dihydropyridine-s[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"HAP1 suppression slows Cav1.2 intracellular trafficking, downregulates Cav1.2 surface expression, reduces Ca influx, and ultimately affects insulin secretion by islet beta cells (Pan et al., 2016)."

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"AC inhibits the expression of CACNA1C, thereby inhibiting Ca from entering cardiomyocytes through LTCC."

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"(2) Patients with diabetes are more prone to AF recurrence because the expression of Kv4.3, Kv1.5, and Cav1.2 in the diabetic myocardium are reduced, which leads to decreased calcium current and potassium current."

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"Functionally, Cav1.2 underlies a slow inward calcium current that sustains depolarization and gives rise to the plateau phase essential for excitation–contraction coupling."