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首页> 外文期刊>Current opinion in lipidology >Very-low-density lipoprotein assembly and secretion.
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Very-low-density lipoprotein assembly and secretion.

机译：低密度脂蛋白的组装和分泌。

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The assembly of apolipoprotein B (apoB) into VLDL is broadly divided into two steps. The first involves transfer of lipid by the microsomal triglyceride transfer protein (MTP) to apoB during translation. The second involves fusion of apoB-containing precursor particles with triglyceride droplets to form mature VLDL. ApoB and MTP are homologs of the egg yolk storage protein, lipovitellin. Homodimerization surfaces in lipovitellin are reutilized in apoB and MTP to achieve apoB-MTP interactions necessary for first step assembly. Structural modeling predicts a small lipovitellin-like lipid binding cavity in MTP and a transient lipovitellin-like cavity in apoB important for nucleation of lipid sequestration. The formation of triglyceride droplets in the endoplasmic reticulum requires MTP however, their fusion with apoB may be MTP-independent. Second step assembly is modulated by phospholipase D and A2. Phospholipases may prime membrane transport steps required for second step fusion and/or channel phospholipids into a pathway for VLDL triglyceride production. The enzymology of VLDL triglyceride synthesis is still poorly understood; however, it appears that ACAT2 is the sole source of cholesterol esters for VLDL and chylomicron assembly. VLDL production is controlled primarily at the level of presecretory degradation. Recently, it was discovered that the LDL receptor modulates VLDL production through its interactions with nascent VLDL in the secretory pathway.
机译：载脂蛋白B（apoB）组装成VLDL大致分为两个步骤。第一个涉及在翻译过程中通过微粒体甘油三酸酯转移蛋白（MTP）将脂质转移至apoB。第二个步骤涉及将含apoB的前体颗粒与甘油三酸酯液滴融合形成成熟的VLDL。 ApoB和MTP是蛋黄存储蛋白lipovitellin的同源物。脂质体中的同质化表面在apoB和MTP中重新使用，以实现第一步组装所必需的apoB-MTP相互作用。结构建模预测MTP中的小脂质体样脂质结合腔和apoB中的短暂脂质体样腔对脂质螯合成核很重要。在内质网中甘油三酸酯液滴的形成需要MTP，但是它们与apoB的融合可能不依赖MTP。第二步组装由磷脂酶D和A2调节。磷脂酶可引发第二步融合所需的膜运输步骤和/或将磷脂引导至VLDL甘油三酸酯生产途径中。 VLDL甘油三酸酯合成的酶学仍知之甚少。然而，看来ACAT2是VLDL和乳糜微粒组装中胆固醇酯的唯一来源。 VLDL的产生主要在分泌前降解的水平上进行控制。最近，发现LDL受体通过其与分泌途径中新生的VLDL的相互作用来调节VLDL的产生。

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