Calcium release from the endoplasmic reticulum through the IP₃ receptor ion channel is strongly regulated by a calcium-binding protein in the lumen of the endoplasmic reticulum.

A new high-throughput method for single-cell RNA-seq in yeast cells shows how stochastic expression of glucose-repressed genes contributes to cell-to-cell differences during adaptation to an environmental change.

Shifts in the balance between nucleotide-favorable and nucleotide-unfavorable conformations of myosin motors encode duty ratios and ADP release rates, demonstrating the power of an ensemble perspective for uncovering sequence-function relationships.

SIMR-1 acts downstream of the piRNA pathway to promote siRNA amplification by the Mutator complex and localizes to perinuclear foci distinct from Mutator foci, P granules and Z granules.

Fluorescent glutamate indicators distort the time course of neurotransmitter diffusion and uptake by competing with transporters, an important caveat to consider when using iGluSnFR and its analogs.

HLA class I-disease associations have been studied for decades; a new approach for investigating the underlying mechanism can overcome past problems with interpretation and help to understand the etiology of human diseases.

Crystallography together with electron-resonance spectroscopy, molecular-dynamics simulations, and transport measurements reveal the molecular details of protein conformational change, and how this change contributes to function in a CLC-type chloride/proton exchanger.

Cell-wide Ca²⁺ signals that regulate numerous cellular functions comprise dual Ca²⁺ release modes through IP₃ receptors, punctate transients mediated by clustered receptors and spatiotemporally diffuse release through functionally distinct receptors.

Two mutations in TRPM3 resulting in developmental and epileptic encephalopathies result in a gain-of-channel function, which may lie at the basis of epileptic activity and neurodevelopmental symptoms in the patients.

The interaction between activated αIIbβ3 on platelets and SLC44A2 on circulating neutrophils facilitates neutrophil capture and drives flow-dependent NETosis.