AP-3 adaptor complex-mediated vesicle trafficking.

Zhuo Ma, Md Nur Islam, Tao Xu, Eli Song
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Abstract

The transport of cargo proteins to specific subcellular destinations is crucial for the different secretory and endocytic traffic pathways. One of the most important steps in maintaining the accuracy of this process is the recruitment of adaptor protein (AP) complexes to the membrane for recognizing and packaging cargo proteins into nascent vesicles. Adaptor protein complex 3 (AP-3) is a heterotetrametric complex implicated in the trafficking of cargo proteins from the trans-Golgi network (TGN) and/or endosomes to lysosomes or lysosome-related organelles (LROs). This complex is also involved in the biogenesis of synaptic vesicles (SVs) in neurons and of dense core vesicles (DCVs) in endocrine cells as well as in the recycling of receptors in immune cells and the regulation of planar cell polarity (PCP) proteins. Functional defects in AP-3 cause multiple abnormalities in cellular vesicle trafficking and related organelle function, leading to various disorders, such as Hermansky-Pudlak syndrome (HPS). However, the molecular mechanism underlying AP-3 has not been fully elucidated, and further investigations are needed to understand AP-3-mediated trafficking, its associated molecules and its related roles in inherited diseases. Here, we review the current understanding of AP-3 in cellular vesicle trafficking, especially focusing on mammalian systems.

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AP-3接头复合物介导的囊泡运输。
货物蛋白运输到特定的亚细胞目的地对于不同的分泌和内吞运输途径至关重要。维持这一过程准确性的最重要步骤之一是将衔接蛋白(AP)复合物募集到膜上,以识别货物蛋白并将其包装到新生囊泡中。接头蛋白复合体3 (AP-3)是一种异四聚体复合体,参与将货物蛋白从反式高尔基网络(TGN)和/或核内体运送到溶酶体或溶酶体相关细胞器(LROs)。该复合物还参与神经元突触囊泡(SVs)和内分泌细胞致密核囊泡(DCVs)的生物发生,以及免疫细胞中受体的再循环和平面细胞极性(PCP)蛋白的调节。AP-3的功能缺陷导致细胞囊泡运输及相关细胞器功能的多重异常,导致多种疾病,如Hermansky-Pudlak综合征(HPS)。然而,AP-3的分子机制尚未完全阐明,需要进一步研究AP-3介导的转运、相关分子及其在遗传性疾病中的相关作用。在这里,我们回顾了目前对细胞囊泡运输中AP-3的理解,特别是在哺乳动物系统中。
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CiteScore
1.30
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117
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