Identification of the monomeric G-protein Rhes as an efaroxan-regulated protein in the pancreatic β-cell

摘要

class="enumerated" style="list-style-type:decimal">Efaroxan induces membrane depolarization by interaction with the pore forming subunit of the ATP-sensitive potassium channel, Kir6.2. However, this effect is not responsible for its full secretory activity.In this study we have used an anti-idiotypic approach to generate antibodies that recognize additional proteins that may be regulated by efaroxan in pancreatic β-cells.Using these antisera in an expression cloning strategy we have identified a monomeric GTP-binding protein, Rhes, as a potential target for regulation by imidazoline ligands. Rhes is shown to be expressed in β-cells and its expression is regulated by efaroxan under conditions when a structurally related molecule, KU14R, is ineffective.The results reveal that β-cells express Rhes and suggest that changes in the expression of this molecule may regulate the sensitivity of β-cells to imidazoline secretagogues.