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Pertussis toxin distinguishes between muscarinic receptor‐mediated inhibition of adenylate cyclase and stimulation of phosphoinositide hydrolysis in Flow 9000 cells
Author(s) -
Lo William W.Y.,
Hughes John
Publication year - 1987
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(87)80894-3
Subject(s) - pertussis toxin , muscarinic acetylcholine receptor , g protein , stimulation , inositol phosphate , cyclase , carbachol , cholera toxin , bordetella pertussis , adenylate cyclase toxin , medicine , chemistry , endocrinology , muscarinic acetylcholine receptor m5 , adenylate kinase , gtp' , muscarinic acetylcholine receptor m1 , inositol , receptor , biology , biochemistry , muscarinic acetylcholine receptor m3 , enzyme , genetics , bacteria
Pretreatment of human embryonic pituitary tumour cells (Flow 9000) with pertussis toxin significantly reduced carbachol‐mediated inhibition of isoprenaline and prostaglandin E 2 stimulation of cyclic AMP formation. This is in accord with an action on the inhibitory G i ‐protein by pertussis toxin. In contrast, pertussis toxin‐pretreatment had no effect on either muscarinic agonist or GTP[S] (a non‐hydrolysable GTP analogue) stimulation of [ 3 H]inositol phosphate production in intact and permeabilized [ 3 H]inositol‐prelabelled Flow 9000 cells, respectively. These results suggest that muscarinic receptors are linked to the inhibition of adenylate cyclase and the stimulation of phosphoinositidase C via two different G‐proteins in Flow 9000 cells.