Cations are essential cofactors in the ATP activation mechanism of the KtrAB cation channel and appear to be cofactors of many other nucleotide-dependent RCK domains.

Molecular dissection of Frizzled, Reck, and Wnt7a provides critical insight into the long-standing question of ligand-receptor specificity in the field of Wnt signaling.

The Rho kinases ROCK1 and 2 act redundantly in regulating cell proliferation and their depletion causes cellular senescence.

The membrane proteins Reck and Gpr124 are integral components of a novel Wnt7a/Wnt7b-specific signaling complex, and there is a distinctive requirement for Wnt/β-catenin signaling in tip cells during angiogenesis in the central nervous system.

Simulations of molecular dynamics suggest how the binding of the β-grasp domain of SUMO1 induces conformational and dynamic effects to activate SENP1.

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.

The discovery of somatostatin-positive inhibitory neurons projecting from mouse cortex to striatum shows that corticostriatal pathways are not exclusively excitatory.