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首页> 外文期刊>Cell metabolism >Rim2alpha determines docking and priming States in insulin granule exocytosis.
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Rim2alpha determines docking and priming States in insulin granule exocytosis.

机译：Rim2alpha确定胰岛素颗粒胞吐作用的对接和启动状态。

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摘要

Insulin secretion is essential for maintenance of glucose homeostasis, but the mechanism of insulin granule exocytosis, the final step of insulin secretion, is largely unknown. Here, we investigated the role of Rim2alpha in insulin granule exocytosis, including the docking, priming, and fusion steps. We found that interaction of Rim2alpha and Rab3A is required for docking, which is considered a brake on fusion events, and that docking is necessary for K(+)-induced exocytosis, but not for glucose-induced exocytosis. Furthermore, we found that dissociation of the Rim2alpha/Munc13-1 complex by glucose stimulation activates Syntaxin1 by Munc13-1, indicating that Rim2alpha primes insulin granules for fusion. Thus, Rim2alpha determines docking and priming states in insulin granule exocytosis depending on its interacting partner, Rab3A or Munc13-1, respectively. Because Rim2alpha(-/-) mice exhibit impaired secretion of various hormones stored as dense-core granules, including glucose-dependent insulinotropic polypeptide, growth hormone, and epinephrine, Rim2alpha plays a critical role in exocytosis of these dense-core granules.
机译：胰岛素分泌对于维持葡萄糖稳态是必不可少的，但是胰岛素颗粒的胞吐作用（胰岛素分泌的最后一步）的机制在很大程度上尚不清楚。在这里，我们研究了Rim2alpha在胰岛素颗粒胞吐作用中的作用，包括对接，引发和融合步骤。我们发现，Rim2alpha和Rab3A的相互作用是停靠所必需的，这被认为是融合事件的刹车，并且停靠对于K（+）诱导的胞吐作用是必需的，而不是葡萄糖诱导的胞吐作用。此外，我们发现通过葡萄糖刺激使Rim2alpha / Munc13-1复合物解离会激活Munc13-1的Syntaxin1，表明Rim2alpha启动了胰岛素颗粒以进行融合。因此，Rim2alpha分别根据其相互作用伴侣Rab3A或Munc13-1确定胰岛素颗粒胞吐作用中的停靠和启动状态。因为Rim2alpha（-/-）小鼠的各种激素（包括葡萄糖依赖性促胰岛素多肽，生长激素和肾上腺素）存储的各种激素的分泌受损，所以Rim2alpha在这些致密颗粒的胞吐作用中起关键作用。

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