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辛德毕斯病毒脂质双层的不对称性。

Asymmetry of the lipid-bilayer of Sindbis virus.

作者信息

Stoffel W, Sorgo W

出版信息

Chem Phys Lipids. 1976 Oct;17(2-3 SPEC NO):324-35. doi: 10.1016/0009-3084(76)90077-3.

DOI:10.1016/0009-3084(76)90077-3
PMID:991384
Abstract

The organization of the lipid bilayer of the enveloped Sindbis virus has been studied. In the model membrane which consists only of two virus specific glycoproteins and host derived lipids the latter were radioactively labelled with 14C-palmitic acid by prelabelling their BHK 21 host cell lipids. The purified virus particles were submitted to neuramidase, bromelain and combromelain-neuraminidase treatment. It could be demonstrated that N-acetyl neuraminic acid residue of the total hematoside present in the virion is hydrolyzed by neuraminidase leaving the particles fully intact. Proteolysis of the spikes leads to particle aggregation yet an unchanged hematoside content. This was fully transformed into ceramidelactoside by subsequent neuraminidase treatment. The analyses of the ceramide species present in hematoside of the control particles and ceramidelactoside derived thereof by neuraminidase hydrolysis are in very close agreement. From these experiments it is concluded that all hematoside molecules are organized in the outer half of the bilayer of the envelope.

摘要

对有包膜的辛德毕斯病毒脂质双层的组织进行了研究。在仅由两种病毒特异性糖蛋白和宿主来源脂质组成的模型膜中,通过对其BHK 21宿主细胞脂质进行预标记,用14C-棕榈酸对后者进行放射性标记。将纯化的病毒颗粒进行神经氨酸酶、菠萝蛋白酶和菠萝蛋白酶-神经氨酸酶处理。可以证明,病毒体中存在的总血苷的N-乙酰神经氨酸残基被神经氨酸酶水解,而颗粒保持完全完整。刺突的蛋白水解导致颗粒聚集,但血苷含量不变。随后的神经氨酸酶处理将其完全转化为神经酰胺乳糖苷。通过神经氨酸酶水解对对照颗粒血苷中存在的神经酰胺种类及其衍生的神经酰胺乳糖苷进行分析,结果非常一致。从这些实验得出结论,所有血苷分子都排列在包膜双层的外半部分。

相似文献

1
Asymmetry of the lipid-bilayer of Sindbis virus.辛德毕斯病毒脂质双层的不对称性。
Chem Phys Lipids. 1976 Oct;17(2-3 SPEC NO):324-35. doi: 10.1016/0009-3084(76)90077-3.
2
Studies on the asymmetric arrangement of membrane-lipid-enveloped virions as a model system.以膜脂包膜病毒粒子的不对称排列作为模型系统的研究。
Hoppe Seylers Z Physiol Chem. 1975 Jul;356(7):1123-9. doi: 10.1515/bchm2.1975.356.2.1123.
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The T=4 envelope of Sindbis virus is organized by interactions with a complementary T=3 capsid.辛德毕斯病毒的T=4包膜是通过与互补的T=3衣壳相互作用而形成的。
Cell. 1987 Mar 27;48(6):923-34. doi: 10.1016/0092-8674(87)90701-x.
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Single amino acid insertions at the junction of the sindbis virus E2 transmembrane domain and endodomain disrupt virus envelopment and alter infectivity.在辛德毕斯病毒E2跨膜结构域和内膜结构域交界处的单个氨基酸插入会破坏病毒包膜并改变感染性。
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Effects of site-directed mutations of transmembrane cysteines in sindbis virus E1 and E2 glycoproteins on palmitylation and virus replication.辛德毕斯病毒E1和E2糖蛋白中跨膜半胱氨酸的定点突变对棕榈酰化和病毒复制的影响。
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Site-directed mutations in the Sindbis virus 6K protein reveal sites for fatty acylation and the underacylated protein affects virus release and virion structure.辛德毕斯病毒6K蛋白的定点突变揭示了脂肪酰化位点,并且酰化不足的蛋白会影响病毒释放和病毒粒子结构。
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Structural characterization of the E2 glycoprotein from Sindbis by lysine biotinylation and LC-MS/MS.通过赖氨酸生物素化和液相色谱-串联质谱法对辛德毕斯病毒E2糖蛋白进行结构表征
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Host modification of Sindbis virus sialic acid content influences alternative complement pathway activation and virus clearance.宿主对辛德毕斯病毒唾液酸含量的修饰影响替代补体途径的激活和病毒清除。
J Immunol. 1981 Nov;127(5):1740-3.

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