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2
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4
Effect and mechanism of phospholipid scramblase 4 (PLSCR4) on lipopolysaccharide (LPS)-induced injury to human pulmonary microvascular endothelial cells.磷脂翻转酶4(PLSCR4)对脂多糖(LPS)诱导的人肺微血管内皮细胞损伤的影响及机制
Ann Transl Med. 2021 Jan;9(2):159. doi: 10.21037/atm-20-7983.
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Herpes simplex viruses activate phospholipid scramblase to redistribute phosphatidylserines and Akt to the outer leaflet of the plasma membrane and promote viral entry.单纯疱疹病毒激活磷脂翻转酶将磷脂酰丝氨酸和 Akt 重分布到质膜的外叶,并促进病毒进入。
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Activation of protein kinase C by phorbol ester increases red blood cell scramblase activity and external phosphatidylserine.佛波酯激活蛋白激酶C可增加红细胞翻转酶活性和外部磷脂酰丝氨酸。
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Lactadherin inhibits secretory phospholipase A2 activity on pre-apoptotic leukemia cells.乳粘连蛋白抑制凋亡前白血病细胞上的分泌型磷脂酶A2活性。
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活化的磷脂翻转酶和受抑制的氨基磷脂转位酶会导致磷脂酰丝氨酸在血小板的一个特定亚群中暴露。

Activated scramblase and inhibited aminophospholipid translocase cause phosphatidylserine exposure in a distinct platelet fraction.

作者信息

Wolfs J L N, Comfurius P, Rasmussen J T, Keuren J F W, Lindhout T, Zwaal R F A, Bevers E M

机构信息

Department of Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht University, P.O. Box 616, 6200 MD, Maastricht, The Netherlands.

出版信息

Cell Mol Life Sci. 2005 Jul;62(13):1514-25. doi: 10.1007/s00018-005-5099-y.

DOI:10.1007/s00018-005-5099-y
PMID:15971000
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11138384/
Abstract

Platelet procoagulant activity is mainly determined by the extent of surface-exposed phosphatidylserine (PS), controlled by the activity of aminophospholipid translocase and phospholipid scramblase. Here, we studied both transport activities in single platelets upon stimulation with various agonists. Besides the formation of procoagulant microparticles, the results show that a distinct fraction of the platelets exposes PS when stimulated. The extent of PS exposure in these platelet fractions was similar to that in platelets challenged with Ca2+-ionophore, where all cells exhibit maximal attainable PS exposure. The size of the PS-exposing fraction depends on the agonist and is proportional to the platelet procoagulant activity. Scramblase activity was observed only in the PS-exposing platelet fraction, whereas translocase activity was exclusively detectable in the fraction that did not expose PS. We conclude that, irrespective of the agonist, procoagulant platelets exhibit maximal surface exposure of PS by switching on scramblase and inhibiting translocase activity.

摘要

血小板促凝活性主要由表面暴露的磷脂酰丝氨酸(PS)的程度决定,而这又受氨基磷脂转位酶和磷脂 scramblase 的活性控制。在此,我们研究了用各种激动剂刺激单个血小板时的这两种转运活性。除了促凝微粒的形成外,结果表明,一部分血小板在受到刺激时会暴露 PS。这些血小板组分中 PS 的暴露程度与用钙离子载体刺激的血小板相似,在这种情况下所有细胞都表现出最大程度的可达到的 PS 暴露。暴露 PS 的组分大小取决于激动剂,并且与血小板促凝活性成正比。仅在暴露 PS 的血小板组分中观察到 scramblase 活性,而转位酶活性仅在未暴露 PS 的组分中可检测到。我们得出结论,无论激动剂如何,促凝血小板通过开启 scramblase 并抑制转位酶活性,使 PS 在表面最大程度地暴露。