IndraLab

Statements

SCN5A activates Ala-Pro. 4 / 4
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"In contrast, expression of SCN5A did not increase the AP upstrokes at these membrane potentials."
22526298
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"SCN5A inactivation defects underlie AP prolongation in LQT3 via gain of function, producing a persistent component of INa termed late current, or INaL."
24892747
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"Mechanism : The basic defect in LQT3 or LQTS-type-3 - which is the third most common LQTS - is caused by an excessive inflow of late Na + current during the plateau, dome or phase 2 of the AP caused by gain-of-function mutations in the SCN5A cardiac Na + channel gene which mediates the fast Nav1.5 current during AP initiation and also late in phase 2 of AP causing an accelerated recovery from inactivation of Na + current as well as AP prolongation, especially at low stimulation rates."
29101013
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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