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PMID: 9665125 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Research Support, U.S. Gov't, P.H.S.

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

Nature ·Vol. 394 ·No. 6688 ·1998-07-02 ·Pages 35-8

Iiri T, Farfel Z, Bourne HR

Abstract

How does a trimeric G 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.

MeSH Terms

GTP-Binding Proteins/genetics,metabolism Guanosine Diphosphate/metabolism Guanosine Triphosphate/metabolism Humans Models, Biological Models, Molecular Mutation Protein Conformation Receptors, Cell Surface/metabolism

Chemicals

Receptors, Cell Surface Guanosine Diphosphate Guanosine Triphosphate GTP-Binding Proteins

Authors & Affiliations

3 authors, click to expand affiliations / ORCID

Iiri T

Department of Cellular and Molecular Pharmacology, University of California, San Francisco 94143-0450, USA.

Farfel Z

Bourne H R

Article Info

Journal

Nature

Abbr.

Nature

ISSN

0028-0836

DOI

10.1038/27831

Published

1998-07-02

Pages

35-8

Language

English

Region

England

NLM ID

0410462

Subset

External Links

PubMed source DOI: 10.1038/27831 View journal details

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