Mutagenesis and activity assays in vitro and in vivo identify residues in the tethered agonist of GPR116, as well as those within the extracellular loops, that are critical for mediating the response to the tethered agonist.

Structural dynamic insights revealed the mechanisms of PC1 activation by stalk-derived peptide agonists which can form a foundation for development of PC1 as a therapeutic target for ADPKD treatment.

Novel components in the pathway from malignant hyperthermia to diabetes include promotion of a kinase that impedes glycogen synthesis, increased lysis of junctophilin1 and gene regulatory actions by a junctophilin fragment, surprisingly predicted to oppose the effects of elevated calcium.