F. Gusovsky, T. Yasumoto, J. Daly
Jan 30, 1989
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Influential Citations
43
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Journal
FEBS Letters
Abstract
Maitotoxin (MTX), a potent marine toxin, elicits a calcium‐dependent activation of cells that can be inhibited by calcium channel blockers like nifedipine. MTX also stimulates phosphoinositide breakdown in smooth muscle cells, NCB‐20 cells and PC12 cells through a nifedipine‐insensitive mechanism. We now report that MTX stimulates phosphoinositide breakdown in a wide variety of cells, and appears to repesent the first general activator of this second messenger‐generating system. MTX‐induced stimulation of phosphoinositide breakdown is dependent in every cell line on the presence of extracellular calcium. In differentiated HL60 cells, in which a chemotactic peptide (fMLP) activates phosphoinositide breakdown via a pertussis toxin‐sensitive mechanism, MTX‐induced stimulation is not affected by pertussis toxin treatment. A phorbol ester has no effect on the response to MTX. Thus, MTX stimulates phosphoinositide breakdown through a calcium‐dependent mechanism that at least in three cell lines (PC12, NCB20 and HL60) is not mediated by a pathway that involves a pertussis toxin‐sensitive guanine nucleotide‐binding protein.