Transient expression of botulinum neurotoxin C1 light chain differentially inhibits calcium and glucose induced insulin secretion in clonal beta-cells

FEBS Letters
J LandC B Wollheim

Abstract

We have investigated the effect of botulinum neurotoxin (BoNT) C1 light chain (LC) on insulin exocytosis from the clonal beta-cell line HIT-T15. In streptolysin-O permeabilized cells, the beta-cell impermeant BoNT C1 cleaved mainly syntaxin 1 and inhibited Ca2+ as well as GTPgammaS induced exocytosis. To study the effect of BoNTs in intact cells, we transiently coexpressed the BoNT LC together with a reporter gene for insulin release. BoNT C1 inhibited K+ induced insulin secretion by 95% but reduced insulin release stimulated by glucose only by 25%. Thus a component of glucose stimulated insulin release is insensitive to BoNT C1.

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Citations

Dec 14, 2001·Biochemical and Biophysical Research Communications·M Ohara-ImaizumiS Nagamatsu
Feb 26, 2004·Proceedings of the National Academy of Sciences of the United States of America·Ester Fernández-SalasK Roger Aoki
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Botulism is a rare but serious paralytic illness caused by a nerve toxin that is produced by the bacterium clostridium botulinum. Discover the latest research on botulism here.

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