GAP-43 augments G protein-coupled receptor transduction in Xenopus laevis oocytes

Stephen M. Strittmatter, Stephen C. Cannon, Elliott M. Ross, Tsutomu Higashijima, Mark C. Fishman

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Abstract

The neuronal protein GAP-43 is thought to play a role in determining growth-cone motility, perhaps as an intracellular regulator of signal transduction, but its molecular mechanism of action has remained unclear. We find that GAP-43, when microinjected into Xenopus laevis oocytes, increases the oocyte response to G protein-coupled receptor agonists by 10- to 100- fold. Higher levels of GAP-43 cause a transient current flow, even without receptor stimulation. The GAP-43-induced current, like receptor-stimulated currents, is mediated by a calcium-activated chloride channel and can be desensitized by injection of inositol 1,4,5-trisphosphate. This suggests that neuronal GAP-43 may serve as an intracellular signal to greatly enhance the sensitivity of G protein-coupled receptor transduction.

Original languageEnglish (US)
Pages (from-to)5327-5331
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume90
Issue number11
DOIs
StatePublished - Jan 1 1993

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