Inhibition of receptor-mediated release of arachidonic acid by pertussis toxin

Gary M. Bokoch, Alfred G. Gilman

Research output: Contribution to journalArticle

217 Citations (Scopus)

Abstract

Treatment of guinea pig neutrophils with pertussis toxin (islet-activating protein; IAP) results in inhibition of N-formyl peptide receptor-mediated release of arachidonic acid and granular enzymes. Inhibition by the toxin is specific, in that responses to the calcium ionophore A23187 are not affected. The action of the toxin is not associated with alterations in cellular concentrations of cyclic AMP but is correlated with the ability of the toxin to catalyze the ADP-ribosylation of a 41,000 dalton membrane protein. This protein comigrates on SDS-polyacrylamide gels with the α subunit of Gi, the inhibitory guanine nucleotide-binding regulatory component of adenylate cyclase. It is likely that this G protein is involved in receptor-mediated signal transduction in neutrophils by mechanisms that do not involve cyclic AMP.

Original languageEnglish (US)
Pages (from-to)301-308
Number of pages8
JournalCell
Volume39
Issue number2 PART 1
DOIs
StatePublished - 1984

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Pertussis Toxin
Arachidonic Acid
Cyclic AMP
Neutrophils
Formyl Peptide Receptor
Signal transduction
Guanine Nucleotides
Calcium Ionophores
Calcimycin
GTP-Binding Proteins
Adenylyl Cyclases
Adenosine Diphosphate
Signal Transduction
Guinea Pigs
Membrane Proteins
Enzymes
Proteins
polyacrylamide gels

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology
  • Medicine(all)

Cite this

Inhibition of receptor-mediated release of arachidonic acid by pertussis toxin. / Bokoch, Gary M.; Gilman, Alfred G.

In: Cell, Vol. 39, No. 2 PART 1, 1984, p. 301-308.

Research output: Contribution to journalArticle

Bokoch, Gary M. ; Gilman, Alfred G. / Inhibition of receptor-mediated release of arachidonic acid by pertussis toxin. In: Cell. 1984 ; Vol. 39, No. 2 PART 1. pp. 301-308.
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