IndraLab

Statements

CACNA1C inhibits pyraclofos. 2 / 2
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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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"We demonstrate that the arrhythmogenic substrate can be studied with clinically available EAM systems and that it may be quantifiable using advanced metrics, such as the RVI, which offers a clinically validated benchmark to test the efficacy of anti-arrhythmic therapies.Since the seminal work by Splawski et al. demonstrated that the p.Gly406Arg mutation in the exon 8A of CACNA1C impairs Ca 1.2 voltage-dependent inactivation, thus substantially prolonging AP duration in cardiomyocytes, notable advances have been made in the understanding of cellular mechanisms of arrhythmogenesis."
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