Tadokoro Satoshi, Hirashima Naohide, Utsunomiya-Tate Naoko
Faculty of Pharma Sciences, Teikyo University.
Biol Pharm Bull. 2016;39(3):446-9. doi: 10.1248/bpb.b15-00751.
Mast cells are involved in allergic responses and undergo exocytotic release of inflammatory mediators in response to antigen stimulation. Soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) proteins are involved in this membrane fusion process; some SNARE-binding proteins regulate SNARE-dependent liposome membrane fusion. SNARE-binding protein complexin II is expressed in mast cells, where it positively regulates exocytotic release after antigen stimulation. We found that complexin II suppressed SNARE-dependent membrane fusion between mast cell SNARE-containing liposomes. This inhibitory effect of complexin II was abolished when we used a structurally divergent mutant (R59H) complexin II, where Arg59 is substituted with histidine. These results suggest that complexin II negatively regulates SNARE-dependent exocytotic membrane fusion in mast cells, and this inhibitory effect is dependent upon Arg59.
肥大细胞参与过敏反应，并在抗原刺激下经历炎性介质的胞吐释放。可溶性N - 乙基马来酰亚胺敏感因子附着蛋白受体（SNARE）蛋白参与这一膜融合过程；一些SNARE结合蛋白调节SNARE依赖性脂质体膜融合。SNARE结合蛋白复合体蛋白II在肥大细胞中表达，在抗原刺激后它正向调节胞吐释放。我们发现复合体蛋白II抑制了肥大细胞含SNARE脂质体之间的SNARE依赖性膜融合。当我们使用结构不同的突变体（R59H）复合体蛋白II（其中精氨酸59被组氨酸取代）时，复合体蛋白II的这种抑制作用被消除。这些结果表明，复合体蛋白II负向调节肥大细胞中SNARE依赖性胞吐膜融合，且这种抑制作用依赖于精氨酸59。
