G-PROTEIN DISEASES FURNISH A MODEL FOR THE TURN-ON SWITCH

How does a trimeric a protein on the inside of a cell membrane respond to activation by a transmembrane receptor? G-protein mutations in pat ients with hypertension and inherited endocrine disorders enhance or b lock signals from stimulated receptors. In combination with three-dime nsional crystal structures and results from biochemical experiments, t he phenotypes produced by these mutations suggest a model for the mole cular activation mechanism that relays hormonal and sensory signals tr ansmitted by many transmembrane receptors.