• Corpus ID: 42101187

Stimulatory effects of maitotoxin on insulin release in insulinoma HIT cells: role of calcium uptake and phosphoinositide breakdown.

@article{Soergel1990StimulatoryEO,
  title={Stimulatory effects of maitotoxin on insulin release in insulinoma HIT cells: role of calcium uptake and phosphoinositide breakdown.},
  author={David G. Soergel and Fabi{\'a}n Gusovsky and Takashi Yasumoto and John W. Daly},
  journal={The Journal of pharmacology and experimental therapeutics},
  year={1990},
  volume={255 3},
  pages={
          1360-5
        }
}
  • D. Soergel, F. Gusovsky, +1 author J. Daly
  • Published 1 December 1990
  • Chemistry, Medicine
  • The Journal of pharmacology and experimental therapeutics
In hamster insulinoma (HIT) cells, maitotoxin (MTX) induces a time-dependent and concentration-dependent release of insulin that requires the presence of extracellular calcium. The response is nearly completely blocked by cinnarizine and cadmium, but is not inhibited by the L-type calcium channel blocker nifedipine or by manganese. MTX induces 45Ca+ uptake in these cells in a dose-dependent mode, and the uptake is blocked with cinnarizine, nifedipine and cadmium, and is partially inhibited by… 
Effect of maitotoxin analogues on calcium influx and phosphoinositide breakdown in cultured cells.
TLDR
The data suggest that the sulfate groups in MTX are important for stimulation of calcium influx and phosphoinositide breakdown, but are not essential for binding to a receptor-site on cell membranes.
Maitotoxin-elicited calcium influx in cultured cells. Effect of calcium-channel blockers.
TLDR
The pattern of inhibition of maitotoxin-elicited calcium influx did not correspond to the ability of the agents to block elevation of calcium that ensues through calcium-release activated calcium (CRAC) channels after activation of phosphoinositide breakdown by ATP in HL-60 cells.
Effects of maitotoxin on calcium entry and phosphoinositidebreakdown in the rabbit ciliated tracheal epithelium
TLDR
Results suggest that MTX independently activates a calcium transport process (which might imply phosphorylation on tyrosine residues) and a PLC not linked to a trimeric G protein.
Maitotoxin-induced calcium entry in human lymphocytes: modulation by yessotoxin, Ca(2+) channel blockers and kinases.
TLDR
MTX produced Ca(2+) influx into human lymphocytes through a SKF96365-sensitive, nifedipine-insensitive pathway, which suggest different pathways to act on [Ca(2+)]i.
Maitotoxin-induced calcium influx in erythrocyte ghosts and rat glioma C6 cells, and blockade by gangliosides and other membrane lipids.
TLDR
Fura-2 experiments suggested that the MTX-induced entry of ions into the ghosts was mediated by a mechanism similar to that reported for cells or tissues, and suggests that removal of oligosaccharides from the cell surface by tunicamycin or capping of sugar chains on plasma membranes by concanavalin A can potentiate the action of MTX.
Insulinotropic Glucagon-like Peptide-1-mediated Activation of Non-selective Cation Currents in Insulinoma Cells Is Mimicked by Maitotoxin*
TLDR
An identity between MTX- and GLP-1-activated currents is supported and it is suggested that protein kinase C may not be involved in the activation of ICa-NS but that it may regulate intracellular Ca2+ release.
Modulation of the maitotoxin response by intracellular and extracellular cations.
TLDR
The results presented here indicated that maitotoxin activates calcium and sodium influx in a concentration-dependent manner and extracellular calcium is required for the sodium influx.
l-cysteine reversibly inhibits glucose-induced biphasic insulin secretion and ATP production by inactivating PKM2
TLDR
Investigation of the effects of prolonged l-cysteine treatment on glucose-stimulated insulin secretion from mouse insulinoma 6 (MIN6) cells and from mouse pancreatic islets found that the treatment reversibly inhibited glucose-induced ATP production and resulting GSIS without affecting proinsulin and insulin synthesis.
Maitotoxin increases voltage independent chloride and sodium currents in GH4C1 rat pituitary cells.
TLDR
A voltage-independent sodium/chloride conductance is identified as an initial action of MTX, one that may promote the sequence of ionic events leading to activation of L-VDCC and massive calcium entry.
Mechanisms underlying the hemolytic and ichthyotoxic activities of maitotoxin.
TLDR
Maitotoxin (MTX), a putative Ca(2+) channel activator produced by the dinoflagellate Gambierdiscus toxicus showed extremely potent hemolytic and ichthyotoxic activities and was 2000 times more toxic to fish than 42-di-hydrobrevetoxin-B (PbTx-3), one of the best known ichysotoxins of red-tide origins.
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