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

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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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"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 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."