G-protein diseases furnish a model for the turn-on switch

被引：162

作者：

Iiri, T

Farfel, Z

Bourne, HR ^{[1
]}

机构：

[1] Univ Calif San Francisco, Dept Mol & Cellular Pharmacol, San Francisco, CA 94143 USA

[2] Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA

[3] Tel Aviv Univ, Biochem Pharmacol Lab, IL-52621 Tel Hashomer, Israel

[4] Tel Aviv Univ, Chaim Sheba Med Ctr, Dept Med E, IL-52621 Tel Hashomer, Israel

来源：

NATURE | 1998年 / 394卷 / 6688期

关键词：

D O I：

10.1038/27831

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

How does a trimeric a protein on the inside of a cell membrane respond to activation by a transmembrane receptor? G-protein mutations in patients with hypertension and inherited endocrine disorders enhance or block signals from stimulated receptors. In combination with three-dimensional crystal structures and results from biochemical experiments, the phenotypes produced by these mutations suggest a model for the molecular activation mechanism that relays hormonal and sensory signals transmitted by many transmembrane receptors.

引用

页码：35 / 38

页数：4

共 45 条

[1] Molecular determinants of selectivity in 5-hydroxytryptamine1B receptor-G protein interactions [J].