Diverse K_ATP channel inhibitors occupy a common binding pocket and stabilize an interaction between Kir6.2 and SUR1 to allosterically control gating and promote the assembly and trafficking of nascent channels.

A structure of a pancreatic ATP-sensitive potassium channel complex at 3.63Å resolution obtained by cryo-electron microscopy reveals how a commonly used anti-diabetic drug interacts with and inhibits the channel to stimulate insulin secretion.

Single-particle cryo-electron microscopy reveals the first subnanometer structure of ATP-sensitive potassium (K_ATP) channels, which provides insight into the structural mechanisms of channel assembly and gating.

Altered activity of ATP-sensitive K⁺ channels underlies the metabolic seizure resistance produced by genetic manipulation of the BAD protein in mice.

In mouse models of Huntington's disease, the subthalamic nucleus, which suppresses movements, also exhibits impaired glutamate homeostasis, NMDA receptor-dependent mitochondrial oxidant stress, firing disruption, and 30% neuronal loss.

A mouse model of human muscle myopathy is used to provide mechanistic insight, identify possible biomarkers of disease, and suggest possible therapeutic strategies to alleviate muscle weakness.

Electron cryo-microscopy has revealed the three-dimensional structure of a potassium channel that has a central role in regulating the release of insulin from the pancreas.

The nerve growth-repellent activity that generates spinal nerve repeat-patterning in birds and mammals is identified at the molecular level, and a similar system is revealed in adult brain grey matter.

MgADP binding to the high-affinity 'consensus' ATPase active site of SUR1 and remodeling of the L0-loop (lasso region) overrides tonic ATP inhibition of KATP channels.

Drosophila HNF4 directs a developmental switch at the onset of adulthood that suppresses diabetes by promoting mitochondrial function and supporting glucose-stimulated insulin secretion.