FEBS Letters | |
Transient expression of botulinum neurotoxin C1 light chain differentially inhibits calcium and glucose induced insulin secretion in clonal β‐cells | |
Wollheim, Claes B1  Zhang, Hui1  Vaidyanathan, Vadakkanchery-Viswanathan3  Sadoul, Karin2  Niemann, Heiner3  Lang, Jochen1  | |
[1] Division de Biochimie Clinique, Département de Médecine Interne, Centre Médical Universitaire, 1 rue Michel Servet, Université de Genève, CH-1211 Geneva 4, Switzerland;Laboratoires de Recherche Louis Jeantet, Centre Médical Universitaire, Université de Genève, Geneva, Switzerland;Institut für Biochemie, Medizinische Hochschule, Hannover, Germany | |
关键词: Exocytosis; Ca2+; Guanosine triphosphate; Glucose; Botulinum neurotoxin C1; Insulin; α/β-SNAP; soluble NSF attachment proteins; BoNT; botulinum neurotoxin; BoNT C1; botulinum neurotoxin C1; BoNT E; botulinum neurotoxin E; eGFP/BoNT C1; enhanced GFP-botulinum neurotoxin C1 fusion protein; NSF; N-ethylmaleimide sensitive factor; phINS; plasmid encoding human insulin; SNARE; soluble NSF attachment receptor; VAMP; vesicle associated membrane protein; | |
DOI : 10.1016/S0014-5793(97)01411-7 | |
学科分类:生物化学/生物物理 | |
来源: John Wiley & Sons Ltd. | |
【 摘 要 】
We have investigated the effect of botulinum neurotoxin (BoNT) C1 light chain (LC) on insulin exocytosis from the clonal β-cell line HIT-T15. In streptolysin-O permeabilized cells, the β-cell impermeant BoNT C1 cleaved mainly syntaxin 1 and inhibited Ca2+ as well as GTPγS 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.
【 授权许可】
Unknown
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