Some evidence suggests the transmembrane protein in GPCRs go back to prokaryotic ion pumping proteins:
So the transmembrane protein can clearly function in other ways than as a receptor. I also read an article a while ago where some species of bacteria had their ATP synthetase genes knocked out, and they survived by getting their ATP from substrate-level phosphorylation. You might wonder how they maintained homeostasis without a functional ATP synthase to regulate proton concentration, and the answer turned out to be that their rhodopsins started translocating ions. Wrote about that here about 2 years ago.