Why the study?
Does cholera toxin pretreatment inhibit receptor-mediated phosphoinositide signaling in human embryonic pituitary cells?
Does cholera toxin pretreatment inhibit receptor-mediated phosphoinositide signaling in human embryonic pituitary cells?
The study suggests the presence of a novel cholera toxin-sensitive G-protein (Gc) responsible for receptor-phosphoinositidase C coupling in human pituitary clonal cells.
Cholera toxin may inhibit pituitary phosphoinositide signaling via a novel G-protein; hypothesis-generating and leaves open relevance to human cells.
Recent studies have implicated that a GTP-binding protein (G-protein) is involved in the coupling of both CCK-8 and muscarinic cholinergic receptors to phosphoinositidase C (PIC) in the human embryonic pituitary cell line, Flow 9000. Pretreatment of these cells with cholera toxin, but not pertussis toxin, inhibited the stimulation of [3H]inositol phosphate production by CCK-8 and acetylcholine. These inhibitory effects of cholera toxin could not be reproduced by treating the cells with the B-subunit of cholera toxin or cAMP-generating agents such as forskolin. These data suggest the presence of a novel Gc protein which is responsible for receptor-PIC coupling in Flow 9000 cells.
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Lo et al. (1987) studied this question.
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