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An Asp 79 Asn mutation of the α 2A ‐adrenoceptor interferes equally with agonist activation of individual G iα ‐family G protein subtypes
Author(s) -
Ward Richard J,
Milligan Graeme
Publication year - 1999
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(99)01581-1
Subject(s) - g protein , mutation , pertussis toxin , receptor , gi alpha subunit , fusion protein , biology , protein subunit , effector , microbiology and biotechnology , genetics , chemistry , gene , recombinant dna
The quantitative effects of an Asp 79 Asn mutation in the porcine α 2A ‐adrenoceptor on adrenaline‐mediated stimulation of the α subunit of individual members of the G i family of G proteins were assessed by measuring GTP turnover number for fusion proteins between the wild type or mutated receptor and pertussis toxin‐resistant forms of each of G i1 , G i2 and G i3 . In each case the receptor mutation limited activation of the G protein to 8–14% of that produced by the wild type receptor. Previous demonstration that in a single cell this mutation selectively interferes with α 2A ‐adrenoceptor regulation of distinct effector end points transduced by G i family members must therefore reflect differential requirements for amplification or the cellular location of individual, co‐expressed, G proteins.