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Maitotoxin, a potent, general activator of phosphoinositide breakdown
Author(s) -
Gusovsky Fabian,
Yasumoto Takeshi,
Daly John W.
Publication year - 1989
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(89)80151-6
Subject(s) - pertussis toxin , activator (genetics) , second messenger system , calcium , calcium channel , extracellular , chemistry , stimulation , microbiology and biotechnology , g protein , biochemistry , receptor , biology , endocrinology , organic chemistry
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.