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病毒诱导的细胞融合的生物化学。膜完整性的变化。

The biochemistry of virus-induced cell fusion. Changes in membrane integrity.

作者信息

Pasternak C A, Micklem K J

出版信息

Biochem J. 1974 Jun;140(3):405-11. doi: 10.1042/bj1400405.

DOI:10.1042/bj1400405
PMID:4374937
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1168017/
Abstract
  1. Phospholipids prelabelled with [(14)C]acetate, [(32)P]phosphate, [(3)H]- or [(14)C]-choline or [(3)H]inositol are not significantly degraded during fusion of Lettrée cells mediated by Sendai virus, nor are carbohydrates prelabelled with [(3)H]fucose, [(14)C]galactose or [(3)H]glucosamine. Less than 1nmol of lysophosphatidylcholine/10(7) cells is formed during fusion. Diethyl p-nitrophenyl phosphate, which inhibits phospholipase A by more than 95% has no effect on fusion. It is concluded that none of the events leading to cell fusion is accompanied by significant turnover of phospholipids or other membrane components. 2. Intracellular K(+) leaks out during virally mediated cell fusion; the loss is not as extensive as that of intracellularly accumulated choline or deoxyglucose. Movement of Ca(2+) into or out of cells could not be detected. 3. At concentrations of Lettrée cells insufficient to be agglutinated by virus, intracellularly accumulated choline and deoxyglucose leak out. Agglutination caused by concanavalin A does not result in leakage of intracellular metabolites. 4. P815Y cells, which agglutinate but do not fuse in the presence of virus, show leakage of intracellularly accumulated metabolites. The extent of leakage does not alter during the G(1) and S periods of the cell cycle. 5. Leakage is inhibited by Ca(2+), but is unaffected by EDTA. 6. It is concluded that the interaction of Sendai virus with mammalian cells causes a weakening of membrane integrity so that intracellular metabolites leak out. Such destabilization may facilitate viral entry and is therefore an interesting system for further biochemical studies.
摘要
  1. 用[¹⁴C]乙酸盐、[³²P]磷酸盐、[³H] - 或[¹⁴C] - 胆碱或[³H]肌醇预标记的磷脂,在仙台病毒介导的莱特里细胞融合过程中不会显著降解,用[³H]岩藻糖、[¹⁴C]半乳糖或[³H]葡糖胺预标记的碳水化合物也不会显著降解。融合过程中形成的溶血磷脂酰胆碱/10⁷个细胞少于1nmol。对磷脂酶A抑制率超过95%的对硝基苯基磷酸二乙酯对融合没有影响。由此得出结论,导致细胞融合的任何事件都不会伴随着磷脂或其他膜成分的显著周转。2. 在病毒介导的细胞融合过程中,细胞内的钾离子会泄漏出来;其损失程度不如细胞内积累的胆碱或脱氧葡萄糖严重。未检测到钙离子进出细胞。3. 在莱特里细胞浓度不足以被病毒凝集时,细胞内积累的胆碱和脱氧葡萄糖会泄漏出来。伴刀豆球蛋白A引起的凝集不会导致细胞内代谢物泄漏。4. P815Y细胞在有病毒存在时会凝集但不融合,显示出细胞内积累的代谢物泄漏。在细胞周期的G₁期和S期,泄漏程度没有改变。5. 泄漏受到钙离子的抑制,但不受乙二胺四乙酸的影响。6. 由此得出结论,仙台病毒与哺乳动物细胞的相互作用会导致膜完整性减弱,从而使细胞内代谢物泄漏出来。这种不稳定可能有助于病毒进入,因此是一个用于进一步生化研究的有趣系统。

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本文引用的文献

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Hemolysis and the release of potassium from cells by Newcastle disease virus (NDV).新城疫病毒(NDV)引起的溶血及细胞内钾离子释放
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Lipids of the adrenal medulla. Lysolecithin, a characteristic constituent of chromaffin granules.肾上腺髓质的脂质。溶血卵磷脂,嗜铬颗粒的一种特征性成分。
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Nature. 1970 Aug 22;227(5260):810-4. doi: 10.1038/227810a0.
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[Lipoid analyses in giant cell formation by herpesvirus hominis].[人疱疹病毒所致巨细胞形成中的类脂分析]
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