Parallel inactivation of α2‐adrenergic agonist binding and Ni by alkaline treatment
- 18 November 1985
- journal article
- Published by Wiley in FEBS Letters
- Vol. 192 (2), 321-325
- https://doi.org/10.1016/0014-5793(85)80134-4
Abstract
α2-Adrenergic receptor-mediated inhibition of adenylate cyclase requires the guanine nucleotide-binding protein, Ni. This protein may also be required for stabilization of high-affinity α2-adrenergic agonist binding. Human platelet membranes treated under alkaline conditions (pH 11.5) exhibited a selective loss of high-affinity agonist binding as measured by P-[3H]aminoclonidine and [3H]UK 14,304. Binding of the antagonist [3H]yohimbine was largely unaffected with retention of > 60% of control binding sites. Ni determined by pertussis toxin-catalyzed [32P]ADP-ribosylation of cholate extracts from alkaline-treated membranes, was also markedly reduced. The parallel loss of of α2-agonist binding and Ni provides additional evidence that Ni, is required for α2-adrenergic agonist binding.Keywords
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