| Literature DB >> 22241937 |
Kathleen Dunlap1, George G Holz, Stanley G Rane.
Abstract
Virtually unknown just a decade ago, GTP-binding proteins (G proteins) have become a major focus of current research. This family of closely related proteins transduce extracellular signals (such as hormones, neurotransmitters and sensory stimuli) into effector responses (1,2). It is now evident that ion channel permeability is one such effector response. In fact, the striking increase in the frequency of reports that demonstrate G protein-regulated ion channel function suggests that channels whose permeability mechanism can be altered by a G protein-mediated process may be more the rule than the exception. It is well-known that the cAMP-dependent modulation of ion channels is under the control of G proteins that regulate adenylate cyclase activity(3,4). However recent studies demonstrate that G proteins also transduce agonist-induced changes in channel activity that do not involve adenylate cyclase. It is on this aspect of G protein signal transduction that this review will focus.Entities:
Year: 1987 PMID: 22241937 PMCID: PMC3254587 DOI: 10.1016/0166-2236(87)90166-4
Source DB: PubMed Journal: Trends Neurosci ISSN: 0166-2236 Impact factor: 13.837