Polyunsaturated fatty acid analogues show selectivity for different cardiac ion channels, suggesting their potential use for the treatment of different subtypes of Long QT Syndrome.

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.

An integrative structural biology approach provides refined models of the KCNQ1-KCNE1 channel complex, which propose a new mechanism to explain how KCNE1 modulates KCNQ1 channel activation.

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.

Personalized heart muscle cells made from stem cells in the laboratory could be used to check an individual’s response to potential new drugs before clinical trials.

The GIRK1 subunit contains a defective Na⁺-binding site but behaves as if it is permanently bound to a sodium ion, and therefore increases the affinity of Gβγ to GIRK1/4 hetero-tetrameric channels in lipid membranes.

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.

X-ray crystallography reveals new conceptual insights into the location of the β2-subunit in the Na_v channel signaling complex.

Restoration of endogenous frataxin levels reverses neurologic and cardiac phenotypes associated with Friedreich's ataxia in adult mice even after significant motor dysfunction.

Evolutionarily conserved hypoxic stress response genes are depleted for association with expression quantitative trait loci.