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CACNA1D activates calcium(2+). 20 / 20
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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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"Cacna1d mediates the entry of calcium into excite cells and participates in various calcium-dependent processes [40]."
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"There is increasing evidence that de novo CACNA1D missense mutations inducing increased Cav1.3 L-type Ca 2+ -channel-function confer a high risk for neurodevelopmental disorders (autism spectrum disorder with and without neurological and endocrine symptoms)."
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"CACNA1D, which was identified in this work as an existing target of calcium channel blockers, is present in the membrane of most excitable cells and mediates calcium influx in response to depolarization(Fourbon et al. 2017)."
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"To date, the single PCa study exploring its protein form, CaV1.3, found it increased Ca i 2+ following androgen stimulation of androgen receptor (AR) positive PCa cell lines [14] ."
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"While highly activated Cav1.3 has been considered to induce higher entry of Ca in noradrenergic and dopaminergic neurons where an oxidative stress is triggered (Hurley et al., 2013), our findings from this mouse model are comparable to the literature (Chan et al., 2007)."
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"As a VGCC, CaV1.3 is expected to promote calcium entry following membrane depolarisation [9] ."
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"Figure 6c (i) shows selected genes involved in Ca signalling that were significantly increased in Brn-3b KO aortas, including CaV channel Cacna1d and S/ER Ca channel RyR2 but also PLN, which inhibits S/ER Ca pump."
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"Cacna1d and Cacnb2, in Brn-3b KO aortas will raise intracellular Ca and trigger contraction in VSMCs by facilitating Ca influx via plasma membrane."
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"Other ion channel genes include CACNA1D, a voltage sensitive calcium channel regulator; KCNJ2, a regulator of potassium ion transport; CHRNG, a nicotinic cholinergic receptor; and MYO1D, a putative binder of calmodulin, which mediates Ca + sensitivity to KCNQ5 ion channels."
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"ERG induced expression of CACNA1D was reported to promote entry of calcium ions into cytosol."
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"Cell based studies demonstrated that activating mutations in the CACNA1D gene can cause increased intracellular Ca 2+ influx, resulting in enhanced aldosterone production XREF_BIBR, XREF_BIBR and inhibitory effect of nifedipine on aldosterone production from H295R cells with mutant Ca v 1.3 was also observed 31."
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"We presume that the reduced expression of CACNA1D in more aggressive prostate cancer and progressors may contribute to decreased Ca 2+ influx and results in the escape of apoptosis, thus suggesting that decreased CACNA1D expression could be a more aggressive phenotype in higher grade prostate cancer or progressors in AS."
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"In the brain such rare CACNA1D variants inducing more subtle changes in Ca v 1.3 function may only be of disease relevance in a permissive genetic background."
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"The Cav1.3 channels are activated at more negative voltages, allowing Ca to flow in under relatively weak depolarizing pulses, and this prolonged inflow of Ca may also have implications for SV development."
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"This is in contrast to SNc neurons, in which the low-threshold L-type Ca channel Cav1.3 activates at subthreshold voltages and mediates most of the Ca influx during pacemaking (Chan et al., 2007; Philippart et al., 2016; Puopolo et al., 2007)."
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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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"Consistent with such observations it has been shown that dopaminergic neurons of the SNc as well as other neuronal populations affected by PD pathology like the locus coeruleus, raphe nuclei or the do[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Rinné et al. conducted a study on a three-generation Turkish family where whole genome sequencing was used to identify a variant of CACNA1D associated with SA dysfunction (Figure 3A) (Rinné et al., 2022) Specifically, examination of exon 22 on the CACNA1D gene led to characterization of the p (Arg930His) variant of the CACNA1D gene, which induces the alteration of the Ca 1.3 long isoform, thus resulting in loss of function of the channel which leads to SANDD."
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"Mechanistically it was reported that ERG induced expression of CACNA1D promoted entry of calcium ions into cytosol [XREF_BIBR]."
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