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SCN5A activates sodium atom. 22 / 22
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"It was previously shown that overexpression of SCN1B and SCN5A, the alpha-subunit of Na v 1.5, increased Na v 1.5 current amplitude and the late sodium current, I NaL XREF_BIBR."
27805004
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"LQT3 is a repolarization disorder caused by gain-of-function mutations in SCN5A encoding the cardiac Na + channel."
23015789
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"Many of the SCN5A variants associated with DCM reduce I Na density or exhibit rate dependent reductions of Na + current (12,24-26)."
22999724
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"The SCN5A gene directs synthesis of cardiac-type, voltage dependent, Na + channels (Na v 1.5), abundant in the heart."
22783200
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"Few months after its identification as a LQTS gene in 1995, it was shown that the SCN5A DeltaKPQ mutation produces the LQTS phenotype by increasing the persistent (or late) Na + inward current and, therefore, prolonging action potential duration."
23684683
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"Co-expression of SCN5A-E1784K and SCN5A-WT reduced I Na, P to 70.03% of WT, shifted steady-state inactivation by -11.03 mV, and increased I Na, L from 0.14% to 1.86% of I Na, P."
27381756
eidos
"Treatment with TTX also significantly reduced the steady-state [ Na + ] i , suggesting that Nav1.5 activity contributes to this elevation of [ Na + ] i ( p < .05 ; n > = 10 ; ANOVA with Tukey test ; Figure 3e ) ."
31612502
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"Loss of function mutations in SCN5A leads to reduced I Na during the AP, causing a reduction in the doming of the AP."
28928611
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"Brugada syndrome (BS) is an inherited cardiac disorder associated with a high risk of sudden cardiac death and is caused by mutations in the SCN5A gene encoding the cardiac sodium channel alpha-subunit (Na (v) 1.5)."
17141278
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"It has been reported that cardiac specific overexpression of the SCN5a gene did not significantly increase the surface density of the Na + channels in ventricular myocytes, indicating that Na V 1.5 localization to the membrane and formation of functional channels are limited [XREF_BIBR]."
24956219
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"Targeting SCN5A expression using specific siRNA completely abolished the presence of I Na and had the same effect as TTX for reducing cancer cell invasiveness."
26283962
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"Plant etal32 previously reported that sleep respiratory abnormality associated intracellular acidosis significantly increased the late I Na caused by the sudden infant death syndrome susceptibility SCN5A common variant, S1103Y, in blacks."
28373245
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"XREF_BIBR Since a synonymous nucleotide change in the SCN5A gene is unlikely to induce a functional change in the Na + channel, a non synonymous substitution was considered as a candidate for the variation associated with this disorder."
26798387
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"Moreover, CPVT was recently linked to a gain-of-function mutation in Scn5a that increased Na + influx by augmenting the Na + channel window current."
28408648
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"Long QT syndrome type 3 (LQT3) is associated with genetic modifications of the Scn5a gene, which interfere with Na + channel inactivation and lead to persistent, arrhythmogenic late Na + currents."
17973950
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"A ground breaking in-vitro expression study by Bennett et al in September 1995 showed that the SCN5A DeltaKPQ mutation produces the LQTS phenotype by increasing the delayed Na + inward current and therefore prolonging the action potential duration."
22895603
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"In the specific case of the S1103Y variant of SCN5A, which has been shown to increase the " late " or sustained Na + current 16, consideration of the use of agents such as ranolazine that diminish the sustained current to reduce arrhythmic events is worthy of speculation."
21498565
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"Taken together, EZH2 is increased in ischemic hearts and epigenetically suppresses Scn5a transcription by H3K27me3, leading to decreased Na V 1.5 expression and Na + channel activity underlying the pathogenesis of arrhythmias."
33370552
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"Mutations in the SCN5A gene associated with LQTS typically cause a gain-of-function phenotype resulting in enhanced Na + entry into the cardiomyocyte during the repolarization period 2."
22138134
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"How does nitrosylation of SCN5A cause increased late I Na?"
23541953
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"The Ala 390 --> Val mutation in alpha-syntrophin alters the inhibitory interaction between nNOS and the plasma membrane Ca-ATPase, and the resultant S nitrosylation of the Na + channel SCN5A enhances Na + influx XREF_BIBR, a pro arrhythmic event recapitulating long-QT syndrome."
20203313
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"Mutations in SCN5A that pathologically increase late I Na may influence repolarization and refractoriness."
25923670