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

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.

journal_name

FEBS Lett

journal_title

FEBS letters

authors

Land J,Zhang H,Vaidyanathan VV,Sadoul K,Niemann H,Wollheim CB

doi

10.1016/s0014-5793(97)01411-7

subject

Has Abstract

pub_date

1997-12-08 00:00:00

pages

13-7

issue

1

eissn

0014-5793

issn

1873-3468

pii

S0014579397014117

journal_volume

419

pub_type

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