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1
Sendai virus-mediated lysis of liposomes requires cholesterol.仙台病毒介导的脂质体裂解需要胆固醇。
Proc Natl Acad Sci U S A. 1983 Mar;80(6):1608-12. doi: 10.1073/pnas.80.6.1608.
2
Effect of lipid composition on HVJ-mediated fusion of glycophorin liposomes to erythrocytes.脂质组成对仙台病毒介导的血型糖蛋白脂质体与红细胞融合的影响。
J Biochem. 1985 May;97(5):1301-10. doi: 10.1093/oxfordjournals.jbchem.a135181.
3
The role of the target membrane structure in fusion with Sendai virus.靶膜结构在与仙台病毒融合中的作用。
Membr Biochem. 1987;7(4):231-47. doi: 10.3109/09687688709029434.
4
Active function of membrane receptors for enveloped viruses. I. Specific requirement for liposome-associated sialoglycolipids, but not sialoglycoproteins, to allow lysis of phospholipid vesicles by reconstituted Sendai viral envelopes.包膜病毒膜受体的活性功能。I. 脂质体相关唾液酸糖脂而非唾液酸糖蛋白对重组仙台病毒包膜裂解磷脂囊泡的特定需求。
Exp Cell Res. 1986 Oct;166(2):279-94. doi: 10.1016/0014-4827(86)90477-5.
5
Fusion of Sendai virus with liposomes: dependence on the viral fusion protein (F) and the lipid composition of liposomes.仙台病毒与脂质体的融合:对病毒融合蛋白(F)和脂质体脂质组成的依赖性。
Virology. 1983 Apr 15;126(1):361-9. doi: 10.1016/0042-6822(83)90485-3.
6
The interaction of Sendai virus with negatively charged liposomes: virus-induced lysis of carboxyfluorescein-loaded small unilamellar vesicles.仙台病毒与带负电荷脂质体的相互作用:病毒诱导的羧基荧光素负载小单层囊泡的裂解
Biochim Biophys Acta. 1985 Oct 24;820(1):1-10. doi: 10.1016/0005-2736(85)90208-1.
7
Glycophorin as a receptor for Sendai virus.血型糖蛋白作为仙台病毒的受体
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8
Sendai virus induced leakage of liposomes containing gangliosides.仙台病毒诱导含有神经节苷脂的脂质体泄漏。
Biochemistry. 1985 Feb 26;24(5):1092-8. doi: 10.1021/bi00326a004.
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Fusion of Sendai virions or reconstituted Sendai virus envelopes with liposomes or erythrocyte membranes lacking virus receptors.仙台病毒粒子或重组仙台病毒包膜与缺乏病毒受体的脂质体或红细胞膜的融合。
J Biol Chem. 1985 Oct 5;260(22):12072-7.
10
Parameters affecting fusion between Sendai virus and liposomes. Role of viral proteins, liposome composition, and pH.影响仙台病毒与脂质体融合的参数。病毒蛋白、脂质体组成和pH值的作用。
Biochemistry. 1986 Dec 16;25(25):8252-60. doi: 10.1021/bi00373a019.

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Single-virus assay reveals membrane determinants and mechanistic features of Sendai virus binding.单病毒分析法揭示了仙台病毒结合的膜决定因素和机制特征。
Biophys J. 2022 Mar 15;121(6):956-965. doi: 10.1016/j.bpj.2022.02.011. Epub 2022 Feb 9.
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Chapter 9 Fusion of Viral Envelopes with Cellular Membranes.第9章 病毒包膜与细胞膜的融合
Curr Top Membr Transp. 1988;32:257-296. doi: 10.1016/S0070-2161(08)60137-9. Epub 2008 May 30.
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Controlled gene and drug release from a liposomal delivery platform triggered by X-ray radiation.基于脂质体的药物传递平台的 X 射线辐射触发的基因和药物可控释放。
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Light-triggered sequence-specific cargo release from DNA block copolymer-lipid vesicles.光触发DNA嵌段共聚物-脂质囊泡的序列特异性货物释放。
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5
Biochemical consequences of a mutation that controls the cholesterol dependence of Semliki Forest virus fusion.控制辛德毕斯病毒融合的胆固醇依赖性的突变的生化后果。
J Virol. 2000 Feb;74(4):1623-31. doi: 10.1128/jvi.74.4.1623-1631.2000.
6
A single point mutation controls the cholesterol dependence of Semliki Forest virus entry and exit.一个单点突变控制着辛德毕斯病毒进入和退出的胆固醇依赖性。
J Cell Biol. 1998 Jan 12;140(1):91-9. doi: 10.1083/jcb.140.1.91.
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Lipid composition and fluidity of the human immunodeficiency virus envelope and host cell plasma membranes.人类免疫缺陷病毒包膜与宿主细胞质膜的脂质组成及流动性
Proc Natl Acad Sci U S A. 1993 Jun 1;90(11):5181-5. doi: 10.1073/pnas.90.11.5181.
8
Role of cholesterol in fusion of Semliki Forest virus with membranes.胆固醇在辛德毕斯病毒与细胞膜融合中的作用。
J Virol. 1984 Oct;52(1):281-3. doi: 10.1128/JVI.52.1.281-283.1984.
9
Membrane fusion of enveloped viruses: especially a matter of proteins.包膜病毒的膜融合:尤其是蛋白质的问题。
J Bioenerg Biomembr. 1990 Apr;22(2):121-55. doi: 10.1007/BF00762943.
10
Cholesterol is required for infection by Semliki Forest virus.胆固醇是辛德毕斯病毒感染所必需的。
J Cell Biol. 1991 Feb;112(4):615-23. doi: 10.1083/jcb.112.4.615.

本文引用的文献

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PHYSICOCHEMICAL PROPERTIES OF OX-BRAIN GANGLIOSIDES.牛脑神经节苷脂的物理化学性质
Biochem J. 1963 Aug;88(2):373-83. doi: 10.1042/bj0880373.
2
A simple method for the isolation and purification of total lipides from animal tissues.一种从动物组织中分离和纯化总脂质的简单方法。
J Biol Chem. 1957 May;226(1):497-509.
3
Serum-induced leakage of liposome contents.血清诱导的脂质体内容物泄漏。
Biochim Biophys Acta. 1980 Apr 10;597(2):418-26. doi: 10.1016/0005-2736(80)90118-2.
4
Tryptophan residues of cholera toxin and its A and B protomers. Intrinsic fluorescence and solute quenching upon interacting with the ganglioside GM1, oligo-GM1, or dansylated oligo-GM1.霍乱毒素及其A和B亚基的色氨酸残基。与神经节苷脂GM1、寡聚GM1或丹磺酰化寡聚GM1相互作用时的固有荧光和溶质猝灭。
J Biol Chem. 1981 Jun 10;256(11):5489-96.
5
pH-dependent fusion between the Semliki Forest virus membrane and liposomes.辛德毕斯病毒膜与脂质体之间的pH依赖性融合。
Proc Natl Acad Sci U S A. 1980 Jun;77(6):3273-7. doi: 10.1073/pnas.77.6.3273.
6
Electron microscopic study on the interaction of Sendai virus with liposomes containing glycophorin.仙台病毒与含血型糖蛋白脂质体相互作用的电子显微镜研究
Biochim Biophys Acta. 1982 Sep 24;691(1):91-6. doi: 10.1016/0005-2736(82)90217-6.
7
Osmotic swelling of phospholipid vesicles causes them to fuse with a planar phospholipid bilayer membrane.磷脂囊泡的渗透性肿胀使其与平面磷脂双分子层膜融合。
Science. 1982 Jul 30;217(4558):458-60. doi: 10.1126/science.6283637.
8
Uncoating of enveloped viruses.包膜病毒的脱壳
Cell. 1982 Jan;28(1):5-6. doi: 10.1016/0092-8674(82)90368-3.
9
Studies on the interaction of HVJ (Sendai Virus) with liposomal membranes. HVJ-induced permeability increase of liposomes containing glycophorin.关于HVJ(仙台病毒)与脂质体膜相互作用的研究。HVJ诱导含血型糖蛋白的脂质体通透性增加。
Virology. 1982 Jan 30;116(2):419-27. doi: 10.1016/0042-6822(82)90136-2.
10
Initiation of fusion and disassembly of Sendai virus membranes into liposomes.仙台病毒膜融合并分解为脂质体的起始过程。
Biochim Biophys Acta. 1981 Aug 6;646(1):31-5. doi: 10.1016/0005-2736(81)90268-6.

仙台病毒介导的脂质体裂解需要胆固醇。

Sendai virus-mediated lysis of liposomes requires cholesterol.

作者信息

Kundrot C E, Spangler E A, Kendall D A, MacDonald R C, MacDonald R I

出版信息

Proc Natl Acad Sci U S A. 1983 Mar;80(6):1608-12. doi: 10.1073/pnas.80.6.1608.

DOI:10.1073/pnas.80.6.1608
PMID:6300860
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC393651/
Abstract

Vesicles were constituted with glycophorin, the Sendai virus receptor of human erythrocytes, and loaded with calcein, a polar derivative of fluorescein, at self-quenching concentrations. On exposure to Sendai virus and mild hypo-osmotic stress, vesicles of the appropriate composition released a significant portion of their internal contents, as indicated by an increase in calcein fluorescence. Susceptible liposomes were not induced to leak by heat-inactivated virus or by trypsin-treated virus. The response of the vesicles to virus attachment is thus analogous to virus-induced hemolysis and presumably involves fusion of the vesicle and virus membranes. In addition to glycophorin and phosphatidylcholine, cholesterol was absolutely required for the lytic response to the virus. The need for cholesterol was not attributable to inactivation of the virus by liposomes without cholesterol. The presence of gangliosides increased the encapsulated volume of the liposomes, but gangliosides did not effectively substitute for glycophorin. Thin-layer chromatography of lipid extracted from incubated virus and liposomes containing a small amount of a fluorescent phosphatidylcholine indicated that phosphatidylcholine in the vesicle is not chemically altered by functional interaction with the virus.

摘要

囊泡由人红细胞的仙台病毒受体血型糖蛋白构成,并装载有处于自猝灭浓度的荧光素的极性衍生物钙黄绿素。在暴露于仙台病毒和轻度低渗应激时,具有适当组成的囊泡释放出其很大一部分内部内容物,钙黄绿素荧光增强表明了这一点。热灭活病毒或经胰蛋白酶处理的病毒不会诱导易感脂质体泄漏。因此,囊泡对病毒附着的反应类似于病毒诱导的溶血,大概涉及囊泡膜与病毒膜的融合。除了血型糖蛋白和磷脂酰胆碱外,胆固醇对于对病毒的裂解反应是绝对必需的。对胆固醇的需求并非归因于不含胆固醇的脂质体使病毒失活。神经节苷脂的存在增加了脂质体的包封体积,但神经节苷脂不能有效地替代血型糖蛋白。从孵育的病毒和含有少量荧光磷脂酰胆碱的脂质体中提取的脂质的薄层色谱表明,囊泡中的磷脂酰胆碱不会因与病毒的功能相互作用而发生化学改变。