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Modulation of mu opioid binding by protein kinase inhibitors
Journal article   Peer reviewed

Modulation of mu opioid binding by protein kinase inhibitors

Vincent J. Aloyo
Biochemical pharmacology, v 49(1)
1995
PMID: 7840778

Abstract

DAMGO mu opioid receptor protein kinase inhibitors
Several isoquinolinesulfonamide protein kinase inhibitors, including 1-(5-isoquinolinesulfonyl) -2-methylpiperazine dihydrochloride (H7), inhibited [ 3H]-[ d-Ala 2,MePhe 4, Gly 5-ol]-enkephalin (DAMGO) binding to rabbit cerebellar mu opioid receptors with K 1 values similar to those reported for kinase inhibition by these compounds, suggesting that their mechanism of action may involve inhibition of protein kinase activity. However, since the binding assays were performed in the absence of exogenous ATP, it is unlikely that protein phosphorylation is taking place during the binding assay, making it improbable that H7 and its congeners inhibit DAMGO binding by inhibition of protein kinase activity. In support of this hypothesis, K252a, a structurally unrelated, broad spectrum, protein kinase inhibitor, was inactive in modulating DAMGO binding, even at a concentration 5-fold greater than its K 1 for inhibiting protein kinase activities. Inhibition of DAMGO binding through inhibition of kinase activity implies a noncompetitive or allosteric mechanism. Scatchard analysis of [ 3H]DAMGO binding combined with Schild analysis demonstrated that the inhibition of DAMGO binding by the isoquinolinesulfonamides was competitive. These results show that the isoquinolinesulfonamide protein kinase inhibitors directly interact with the mu opioid receptor. Thus, these compounds are unsuitable for the investigation of the potential role of protein phosphorylation in the modulation of mu opioid receptor binding.

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