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首页> 外文期刊>Biology Open >Phospholipase C-related catalytically inactive protein (PRIP) controls KIF5B-mediated insulin secretion
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Phospholipase C-related catalytically inactive protein (PRIP) controls KIF5B-mediated insulin secretion

机译：磷脂酶C相关的催化失活蛋白（PRIP）控制KIF5B介导的胰岛素分泌

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We previously reported that phospholipase C-related catalytically inactive protein (PRIP)-knockout mice exhibited hyperinsulinemia. Here, we investigated the role of PRIP in insulin granule exocytosis using Prip -knockdown mouse insulinoma (MIN6) cells. Insulin release from Prip -knockdown MIN6 cells was higher than that from control cells, and Prip knockdown facilitated movement of GFP-phogrin-labeled insulin secretory vesicles. Double-immunofluorescent staining and density step-gradient analyses showed that the KIF5B motor protein co-localized with insulin vesicles in Prip -knockdown MIN6 cells. Knockdown of GABAA-receptor-associated protein (GABARAP), a microtubule-associated PRIP-binding partner, by Gabarap silencing in MIN6 cells reduced the co-localization of insulin vesicles with KIF5B and the movement of vesicles, resulting in decreased insulin secretion. However, the co-localization of KIF5B with microtubules was not altered in Prip - and Gabarap -knockdown cells. The presence of unbound GABARAP, freed either by an interference peptide or by Prip silencing, in MIN6 cells enhanced the co-localization of insulin vesicles with microtubules and promoted vesicle mobility. Taken together, these data demonstrate that PRIP and GABARAP function in a complex to regulate KIF5B-mediated insulin secretion, providing new insights into insulin exocytic mechanisms.
机译：我们以前报道过磷脂酶C相关的催化失活蛋白（PRIP）敲除小鼠表现出高胰岛素血症。在这里，我们调查了PRIP在使用Prip敲低小鼠胰岛素瘤（MIN6）细胞的胰岛素颗粒胞吐作用中的作用。从敲除MIN6细胞中释放的胰岛素高于从对照细胞释放出来的胰岛素，而敲除MIN1细胞促进了GFP-凝集素标记的胰岛素分泌囊泡的运动。双重免疫荧光染色和密度逐步梯度分析表明，KIF5B运动蛋白与胰岛素小泡在Prip-knockdown MIN6细胞中共定位。 Gabarap沉默在MIN6细胞中敲低GABAA受体相关蛋白（GABARAP），一种微管相关的PRIP结合伴侣，降低了胰岛素囊泡与KIF5B的共定位以及囊泡的运动，导致胰岛素分泌减少。然而，在Prip-和Gabarap-敲低细胞中，KIF5B与微管的共定位没有改变。 MIN6细胞中通过干扰肽或Prip沉默释放的未结合GABARAP的存在增强了胰岛素囊泡与微管的共定位并促进了囊泡迁移。综上所述，这些数据表明PRIP和GABARAP在复合物中发挥功能，以调节KIF5B介导的胰岛素分泌，从而为胰岛素胞外机制提供新见解。

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