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Pre-existing membrane complexes, permanence of inactive G protein in the vicinity of GPCRs as well as co-association of Gs and -arrestin to the GLP-1R would be consistent with the discrete fold-increase in exendin-mediated Gs recruitment observed compared to that of -arrestin2 and might contribute to explain the observed independence of Gs association from the recruitment of GRK2 and binding of -arrestin, at least in model experimental systems involving overexpression of receptor and partner proteins