Is lipid translocation involved during endo- and exocytosis?

Is lipid translocation involved during endo- and exocytosis?
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DOI:
10.1016/s0300-9084(00)00209-1
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发表时间:
2000-05-01
期刊:
影响因子:
3.9
通讯作者:
Devaux, PF
Devaux, PF
中科院分区:
生物学3区
文献类型:
--
作者:
Devaux, PF

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氨基磷脂移位酶负责将磷脂酰丝氨酸和磷脂酰乙醇胺从质膜的外叶转运至内叶,刺激氨基磷脂移位酶可引起红细胞中的内吞样囊泡并刺激K562细胞中的内吞作用。在这篇文章中的论点,支持的想法,积极运输的脂质可能是驱动力参与膜折叠的早期步骤的内吞作用。该模型是持续的纯脂质囊泡的形状变化引发的内部和外部脂质的比例变化的实验。结果表明,由质膜脂质易位引起的直径为100-200 nm的微泡的形成暗示了整个膜中的表面张力。很可能是细胞骨架蛋白和内部细胞器阻止了真实的细胞发生巨大单层囊泡所见的整体形状变化。本文提出的另一个假设是,在胞吐过程中可能存在磷脂“乱序酶”,这可能有利于微泡的展开。(C)2000年法国生物化学和生物分子学会/科学和医学版Elsevier SAS。
Stimulation of the aminophospholipid translocase, responsible for the transport of phosphatidylserine and phosphatidylethanolamine from the outer to the inner leaflet of the plasma membrane, provokes endocytic-like vesicles in erythrocytes and stimulates endocytosis in K562 cells. In this article arguments are given which support the idea that the active transport of lipids could be the driving force involved in membrane folding during the early step of endocytosis. The model is sustained by experiments on shape changes of pure lipid vesicles triggered by a change in the proportion of inner and outer lipids. It is shown that the formation of microvesicles with a diameter of 100-200 nm caused by the translocation of plasma membrane lipids implies a surface tension in the whole membrane. It is likely that cytoskeleton proteins and inner organelles prevent a real cell from undergoing overall shape changes of the type seen with giant unilamellar vesicles. Another hypothesis put forward in this article is the possible implication of the phospholipid 'scramblase' during exocytosis which could favor the unfolding of microvesicles. (C) 2000 Societe francaise de biochimie et biologie moleculaire / Editions scientifiques et medicales Elsevier SAS.