Cell
ArticleInhibition of receptor-mediated release of arachidonic acid by pertussis toxin
References (51)
- et al.
Activation of the inhibitory GTP-binding protein of adenylate cyclase, Gi, by β-adrenergic receptors in reconstituted phospholipid vesicles
J. Biol. Chem.
(1984) - et al.
Demonstration of a receptor on rabbit neutrophils for chemotactic peptides
Biochem. Biophys. Res. Commun.
(1977) - et al.
Inhibition of the neutrophil oxidative response to a chemotactic peptide by inhibitors of arachidonic acid oxygenation
Biochem. Biophys. Res. Commun.
(1979) - et al.
Identification of the predominant substrate for ADP-ribosylation by islet activating protein
J. Biol. Chem.
(1983) - et al.
Purification and properties of the inhibitory guanine nucleotide-binding regulatory component of adenylate cyclase
J. Biol. Chem.
(1984) - et al.
Chemotactic peptide stimulated endogenous arachidonic acid metabolism in HL60 granulocytes
Biochem. Biophys. Res. Commun.
(1981) - et al.
A ternary complex model explains the agonist-specific binding properties of the adenylate cyclase-coupled β-adrenergic receptor
J. Biol. Chem.
(1980) - et al.
Modification by islet-activating protein of receptor-mediated regulation of cyclic AMP accumulation in isolated rat heart cells
J. Biol. Chem.
(1981) - et al.
Islet activating protein
- et al.
Slow interaction of islet-activating protein with pancreatic islets during primary culture to cause reversal of α-adrenergic inhibition of insulin secretion
J. Biol. Chem.
(1980)
ADP-ribosylation of the specific membrane protein of C6 cells by islet-activating protein associated with modification of adenylate cyclase activity
J. Biol. Chem.
The inhibitory guanine nucleotide-binding regulatory component of adenylate cyclase
The inhibitory guanine nucleotide-binding regulatory component of adenylate cyclase
Specific uncoupling by islet-activating protein, pertussis toxin, of negative signal transduction via α-adrenergic, cholinergic, and opiate receptors in neuroblastoma X glioma hybrid cells
J. Biol. Chem.
Roles of phospholipid metabolism in secretory cells
Loss of the inhibitory function of the guanine nucleotide regulatory component of adenylate cyclase due to its ADP-ribosylation by islet activating protein, pertussis toxin, in adipocyte membranes
J. Biol. Chem.
Arachidonic acid induced degranulation of rabbit peritoneal neutrophils
Biochem. Biophys. Res. Commun.
Suppression of passive cutaneous anaphylaxis by pertussis toxin, an islet-activating protein, as a result of inhibition of histamine release from mast cells
Biochem. Pharmacol.
The biochemical basis of phagocytosis. I. Metabolic changes during the ingestion of particles by polymorphonuclear leukocytes
J. Biol. Chem.
Requirements for cholera toxin-dependent ADP-ribosylation of the purified regulatory component of adenylate cyclase
J. Biol. Chem.
Binding of the chemotactic synthetic peptide [3H]formyl-Nor-Leu-Leu-Phe to plasma membrane of rabbit neutrophils
FEBS Lett.
Stimuli which provoke secretion of azurophil enzymes from human neutrophils induce increments in adenosine cyclic 3′,5′-monophosphate
Biochim. Biophys. Acta
Reconstitution of catecholaminesensitive adenylate cyclase
Regulation of glycogen metabolism in polymorphonuclear leukocytes
J. Biol. Chem.
Mechanism of arachidonic acid release in human polymorphonuclear leukocytes
Biochem. Biophys. Acta
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