IndraLab

Statements


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"For example, Itoh et al. reported that the SCN5A variant p.N406S identified in Brugada Syndrome patients enhanced use dependent block of sodium currents with quinidine, a class IA antiarrythmic agent, but the same variant abolished the block with pilsicainide [XREF_BIBR]."

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"In the Brugada syndrome, mutations in SCN5A reduce sodium current density, causing premature repolarization of the epicardial action potential due to an all or none repolarization at the end of phase 1."

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"Perspectives COMPETENCY IN MEDICAL KNOWLEDGE : BrS is commonly associated with genetic variants in SCN5A that reduce inward sodium current and promote single-cell proarrhythmic activity."

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"The HERG mediated potassium and the SCN5A mediated sodium currents, however, were only slightly reduced by estradiol at concentrations of up to 30 microM."

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"Mutations in SCN5A may cause sodium channel dysfunction by decreasing peak sodium current, which slows conduction and facilitates reentry based arrhythmias, and by enhancing late sodium current, which prolongs the action potential and sets the stage for early afterdepolarization and arrhythmias."

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"We report identification and characterization of a rare loss-of-Function (LoF) variant in the SCN5A gene that impaired sodium current density and was associated with incessant and lethal ventricular tachycardia and fibrillation (VT/VF) after administration of lidocaine to a patient with acute myocardial infarction (AMI)."

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"Variants in SCN5A have been shown to impair the sodium ion channel and associated with dilated cardiomyopathy with and without conduction disease, Brugada syndrome, and other arrhythmias."

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"XREF_BIBR SCN5A causes slow recovery of the sodium channels from an inactive state, which contributes to a conduction delay at the ventricular level."

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"Zfhx3 Transcription Factor Represses the Expression of SCN5A Gene and Decreases Sodium Current Density (INa)."

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"Specially, the cardiac sodium channel (SCN5A) mutations that reduce peak sodium current (such as mutations linked to Brugada syndrome) and QTc prolongation in patients with LQT3, or overlap syndrome."

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"Deficient SCN5A gene mutation could decrease the function of sodium channel, decrease the I Na at depolarization and depolarization velocity and peak value of cardiomyocytes during depolarization, and block the cardiac conduction system in varying degrees, eventually leading to the occurrence of AVB [XREF_BIBR]."