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SCN5A inhibits sodium(1+). 13 / 13
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"geographusNaV1.2, NaV1.4, not completely determinedchannels, m-conotoxins block vertebratemuscle and nerve sodium channels, s-conotoxins inhibit 5HT3 are potential novel analgesics that are currently under investiga-channel, y-conotoxins non competitively block neuromuscular tion."
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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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"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]."
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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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"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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"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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"Zfhx3 Transcription Factor Represses the Expression of SCN5A Gene and Decreases Sodium Current Density (INa)."
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"SCN5A p.R1865H reduced the instability index of Na 1.5 protein and sodium current."
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"Several case studies have reported that SCN5A pore variants cause a stronger reduction in the sodium current in heterologous expression systems [49,50]."
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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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"Moreover, the ATII-induced production of H O triggers the binding action of nuclear factor kappa B (NF-κB) to the sodium channel protein type 5 subunit alpha (SCN5A), reducing the inward current of sodium (INa)."
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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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"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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