ML277 exclusively enhances the AO state voltage-sensing domain (VSD)-pore coupling of KCNQ1 channels, providing an effective tool to investigate the voltge-dependent gating and new strategies for treating long QT syndrome.

The I_Ks potassium channel complex displays functional flexibility that depends on the ratio of its constituent KCNQ1 and KCNE1 protein subunits.

An auxiliary subunit alters the effect of a family of small-molecule openers on a voltage-gated potassium channel by inducing structural re-arrangements that promote protonation of the drug molecule.

Contrary to a generally accepted principle, the pore properties of KCNQ1 channels depend on the states of voltage-sensing domains activation; KCNE1 alters the voltage-sensing domains-pore coupling to modulate KCNQ1 channel properties.

Fatty acid analogues are interesting prototype compounds that may inspire the development of future I_Ks channel activators to treat patients with long QT syndrome caused by diverse arrhythmia-causing mutations in the I_Ks channel.

Sodium-activated potassium ion currents encoded by the kcnt1 gene delay action potential firing in DRG neurons by activity preceding an action potential.

A potassium channel, as a nonconducting function, organizes compartmentalized neuronal calcium signaling microdomains via structural and functional coupling of plasma membrane and endoplasmic reticulum calcium channels.

Coordinated microRNAs activity induced by VEGF represses cell proliferation and favors cell migration at the onset of sprouting angiogenesis in endothelial cells.

The control of local cell properties such as epithelial cell number and mechanical force production by Hippo signaling is a major determinant of lung branching.