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The function of apolipoproteins L (APOLs): relevance for kidney disease, neurotransmission disorders, cancer and viral infection.
The FEBS Journal ( IF 5.5 ) Pub Date : 2020-06-12 , DOI: 10.1111/febs.15444
Etienne Pays 1
Affiliation  

The discovery that apolipoprotein L1 (APOL1) is the trypanolytic factor of human serum raised interest about the function of APOLs, especially following the unexpected finding that in addition to their protective action against sleeping sickness, APOL1 C‐terminal variants also cause kidney disease. Based on the analysis of the structure and trypanolytic activity of APOL1, it was proposed that APOLs could function as ion channels of intracellular membranes and be involved in mechanisms triggering programmed cell death. In this review, the recent finding that APOL1 and APOL3 inversely control the synthesis of phosphatidylinositol‐4‐phosphate (PI(4)P) by the Golgi PI(4)‐kinase IIIB (PI4KB) is commented. APOL3 promotes Ca2+‐dependent activation of PI4KB, but due to their increased interaction with APOL3, APOL1 C‐terminal variants can inactivate APOL3, leading to reduction of Golgi PI(4)P synthesis. The impact of APOLs on several pathological processes that depend on Golgi PI(4)P levels is discussed. I propose that through their effect on PI4KB activity, APOLs control not only actomyosin activities related to vesicular trafficking, but also the generation and elongation of autophagosomes induced by inflammation.

中文翻译:


载脂蛋白 L (APOL) 的功能:与肾脏疾病、神经传递障碍、癌症和病毒感染的相关性。



载脂蛋白 L1 (APOL1) 是人血清中的锥虫分解因子,这一发现引起了人们对 APOL 功能的兴趣,特别是在意外发现 APOL1 C 末端变异除了对昏睡病具有保护作用外,还会引起肾脏疾病。基于对APOL1的结构和锥虫分解活性的分析,提出APOL可以作为细胞内膜的离子通道并参与触发细胞程序性死亡的机制。在这篇综述中,对最近发现的 APOL1 和 APOL3 反向控制高尔基体 PI(4) 激酶 IIIB (PI4KB) 合成磷脂酰肌醇 4-磷酸 (PI(4)P) 的情况进行了评论。 APOL3 促进 PI4KB 的 Ca 2+依赖性激活,但由于它们与 APOL3 的相互作用增加,APOL1 C 末端变体可以使 APOL3 失活,导致高尔基体 PI(4)P 合成减少。讨论了 APOL 对取决于高尔基体 PI(4)P 水平的几种病理过程的影响。我认为,通过对 PI4KB 活性的影响,APOL 不仅控制与囊泡运输相关的肌动球蛋白活性,还控制炎症诱导的自噬体的产生和延伸。
更新日期:2020-06-12
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