IndraLab

Statements


INS inhibits KCNQ1. 6 / 6
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"We found that insulin suppressed KCNQ1 / KCNE1 currents, in which KCNE1 played an essential role in the effects of insulin.3 The phosphatidylinositol 3kinase (PI3K)/Akt pathway was responsible for the effects of insulin, while the MEK and ERK pathway was not."

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"A hypothetical model of insulin mediated suppression of KCNQ1 and KCNE1 currents."

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"Insulin substitution fully prevented the diabetes induced changes in I (Ks), KvLQT1 and MinK, however, the changes in I (to), Kv4.3, and Kv1.4 were only partially diminished by insulin."

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"Acute application of insulin suppressed the KCNQ1 and KCNE1 currents and phosphorylated Akt and extracellular signal regulated kinase (ERK), the two major downstream effectors, in a concentration dependent manner."

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"Insulin suppresses IKs (KCNQ1 and KCNE1) currents, which require beta-subunit KCNE1."

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"We have previously reported that acute application of insulin suppresses the KCNQ1 and KCNE1 currents that play an important role in terminating ventricular action potential."