Characterization of Ca²⁺ selectivity and non-conductance mechanism induced by pore mutation N617D in the skeletal muscle DHPR.

Determination of a model of mitochondrial protein import elucidated using a high-resolution transport assay and kinetic modelling.

A computational method for predicting evolutionary pathways to antimicrobial resistance, accounting for how epistatic interactions determine trajectories, is described.

Transient weakness in myotonia congenita is caused by depolarization secondary to activation of persistent Na⁺ current in skeletal muscle.

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.

Channel characteristics of the presequence translocation pore have a direct impact on protein import into the mitochondrial matrix.

Non-synaptic extracellular vesicles may be involved in the release of endogenous cannabinoids in the central nervous system thereby representing a novel mechanism to mediate their effects on synaptic transmission.

The ABO and RhD blood groups are associated with disease-wide susceptibility differences.

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.

The motor that drives preproteins into the mitochondrial matrix is coupled to the translocase by Tim44, a two-domain scaffold protein with an intrinsically disordered "dynamic arm" and a structurally stable anchoring domain.