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Stimulation of cAMP accumulation by the cloned Xenopus melatonin receptor through G i and G z proteins
Author(s) -
Yung Lisa Y.,
Tsim Siu-Tai,
Wong Yung H.
Publication year - 1995
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 - 10.1016/0014-5793(95)00963-a
Subject(s) - pertussis toxin , melatonin , adenylyl cyclase , melatonin receptor , gs alpha subunit , receptor , g protein , gi alpha subunit , biology , xenopus , medicine , transfection , endocrinology , hek 293 cells , stimulation , microbiology and biotechnology , cell culture , biochemistry , genetics , gene
The Xenopus melatonin receptor was expressed in human embryonic kidney 293 cells and assayed for cAMP accumulation. In transfected 293 cells expressing the melatonin receptor, melatonin dose‐dependently inhibited the endogenous adenylyl cyclases. In contrast, melatonin stimulated the accumulation of cAMP in cells co‐expressing the type II adenylyl cyclase. Both the inhibitory and stimulatory responses to melatonin were mediated via G i ‐like proteins as they were blocked by pertussis toxin. Upon co‐transfection with the α subunit of G z , the ability of melatonin to regulate both type II and the endogenous adenylyl cyclases became refractory to pertussis toxin, indicating that the melatonin receptor can also couple to G z . However, other pertussis toxin‐insensitive G proteins such as G q , G 12 and G 13 were unable to interact with the melatonin receptor.