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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Cholera toxin ADP-ribosylates the receptor-coupled form of pertussis toxin-sensitive G-proteins.

Cholera toxin catalyzes the ADP-ribosylation of 40 kDa pertussis toxin substrates in membranes from NG108-15 cells, which is increased in the presence of the opioid agonist DADLE. The basal ADP-ribosylation can be abolished by the opioid antagonist ICI 174864, suggesting that unoccupied opioid receptors interact spontaneously with the pertussis toxin substrates Gi/Go in the membrane. Treatment of NG108-15 cells with the opioid agonist DADLE leads to a reduction of agonist-stimulated and basal ADP-ribosylation of 40 kDa substrates catalyzed by cholera toxin. This indicates that the spontaneous interaction between opioid receptors and G-proteins is decreased in membranes of cells in which the receptor was desensitized by prolonged exposure to the agonist.[1]


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