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"Furthermore, while the I Ks current suppressing effect is mediated by KCNQ1, the voltage-shift effect requires the presence of KCNE1, because JPH-2 does not shift the activation curve of KCNQ1 expressed alone."

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"PKA phosphorylation of KCNQ1 increases the I KS current to enhance relaxation of muscle in response to increased heart rate."

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"The coassembly of KCNQ1 and KCNE1 produces the I KS potassium current that is critical for the late repolarization of the cardiac action potential."

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"The delayed rectifier K + channels K V 7.1 (KCNQ1), which underlies I Ks, and K V 11.1 (ERG), which produces I Kr, are thought to be primarily responsible for repolarization of the sinoatrial AP."

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"PKA phosphorylates Ser27 on KCNQ1 to modulate I Ks and phosphorylates Ser43 of Yotiao to further enhance regulation by the sympathetic nervous system, whereas dephosphorylation of these sites and suppression of I Ks currents are facilitated by anchored PP1."

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"It was subsequently shown that a complex of the KCNQ1 pore forming subunit with KCNE1 underlies I Ks."

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"Presumably, loss-of-function mutations in KCNQ1 reduce the ability to increase I Ks and, thereby, to sufficiently counteract the effect of the increased I CaL under conditions with an increased adrenergic tonus."

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"The overexpression of miR-1/133 suppressed KCNE1 and KCNQ1, which both encode the slow delayed rectifier potassium current (I Ks), playing a key role in restoring the functional I Ks, which is reduced by the inhibition of KCNE1 and KCNQ1 in diabetic conditions [XREF_BIBR]."

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"This hypothesis was confirmed by us [61] and others [60] when heterologous expression of KCNQ1 subunits with minK subunits in mammalian cells was shown to induce I Ks."

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"It is well known that the congenital dysfunction of I Ks caused by genetic mutations in the KCNQ1 or KCNE1 gene is linked to congenital long QT syndrome subtype LQT1 or LQT5 [XREF_BIBR]."

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"beta1-AR activation leads to activation of protein kinase A (PKA), which directly phosphorylates the KCNQ1 subunit, increasing I Ks function."

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"The founder of this family, KCNE1, also known as MinK (minimal K + channel protein), or IsK, was first found to co-assemble with the Kv alpha subunit Kv7.1 (KCNQ1) to form the slowly activating cardiac ventricular repolarization current I Ks."

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"Mutations in the KCNQ1 and HERG genes cause the Long QT Syndromes, LQTS1 and LQTS2, due to reductions in the cardiac repolarizing I Ks and I Kr currents, respectively."

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"Furthermore, they showed that this was because of their ability to regulate the expression of 2 potassium channel proteins, KCNE1 (P15382) and KCNQ1 (P51787), which mediate I Ks."

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"As shown in Figure 3A, coexpression of KCNQ1 -WT (0.5 mug) with KCNE1 (0.5 mug) produced a slowly activating outward WT-I Ks on depolarization to 30 mV from the holding potential of -80 mV."

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"4,16,19-21 Chen et al 4 first reported the KCNQ1 -S140G mutation that potentiated I Ks, especially the component of instantaneous activation."

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"These results show that Ca 2+, CaM, or binding of Ca 2+ / CaM complex to the C terminus of KCNQ1 is required to activate I Ks."

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"Mutations in KCNQ1 can cause dysfunction in the I Ks channel, such as a delay in channel opening or a reduction in the duration for which it is open XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR."

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"The subunits KCNQ1 and KCNE1 generate the slowly activating, delayed rectifier potassium current, I Ks, that responds to sympathetic stimulation and is critical for human cardiac repolarization."

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"Under basal conditions, only a small portion of KCNQ1 reaches the cell surface to support the I Ks function."

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"Given potential variability between experiments, controls were assessed during the time of each experimental group and the ratio of KCNQ1 to KCNE1 was standardized to produce classical characteristics[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"