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脊髓灰质炎病毒蛋白酶3C（P3-7c）不会切割真核生物mRNA帽结合蛋白复合物的P220。

Poliovirus protease 3C (P3-7c) does not cleave P220 of the eucaryotic mRNA cap-binding protein complex.

作者信息

Lee K A, Edery I, Hanecak R, Wimmer E, Sonenberg N

出版信息

J Virol. 1985 Aug;55(2):489-93. doi: 10.1128/JVI.55.2.489-493.1985.

DOI:10.1128/JVI.55.2.489-493.1985
PMID:2991572
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC254958/
Abstract

Infection of HeLa cells by poliovirus results in proteolysis of the large subunit (P220) of the cap-binding protein complex. This is believed to cause the rapid shut-off of host protein synthesis during poliovirus infection. In this communication we examined the possible involvement of poliovirus proteins 3C (a proteinase) and 2C in cleavage of P220. Using antisera against these two viral polypeptides, we were unable to inhibit proteolysis of P220 in an in vitro assay. These results indicate that viral proteins 3C and 2C are not directly involved in cleaving P220 and hence do not cause shut-off of cellular protein synthesis.

摘要

脊髓灰质炎病毒感染HeLa细胞会导致帽结合蛋白复合体的大亚基（P220）发生蛋白水解。据信，这会导致脊髓灰质炎病毒感染期间宿主蛋白质合成的迅速停止。在本通讯中，我们研究了脊髓灰质炎病毒蛋白3C（一种蛋白酶）和2C在P220裂解过程中可能的作用。使用针对这两种病毒多肽的抗血清，我们无法在体外试验中抑制P220的蛋白水解。这些结果表明，病毒蛋白3C和2C不直接参与裂解P220，因此不会导致细胞蛋白质合成的停止。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d6a/254958/d9e4bf915c8a/jvirol00119-0246-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d6a/254958/5e937e676715/jvirol00119-0244-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d6a/254958/5606118384a4/jvirol00119-0245-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d6a/254958/d9e4bf915c8a/jvirol00119-0246-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d6a/254958/5e937e676715/jvirol00119-0244-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d6a/254958/5606118384a4/jvirol00119-0245-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d6a/254958/d9e4bf915c8a/jvirol00119-0246-a.jpg

相似文献

1
Poliovirus protease 3C (P3-7c) does not cleave P220 of the eucaryotic mRNA cap-binding protein complex.脊髓灰质炎病毒蛋白酶3C（P3-7c）不会切割真核生物mRNA帽结合蛋白复合物的P220。
J Virol. 1985 Aug;55(2):489-93. doi: 10.1128/JVI.55.2.489-493.1985.
2
Poliovirus protease does not mediate cleavage of the 220,000-Da component of the cap binding protein complex.脊髓灰质炎病毒蛋白酶不介导帽结合蛋白复合体220,000道尔顿成分的切割。
Proc Natl Acad Sci U S A. 1985 May;82(9):2723-7. doi: 10.1073/pnas.82.9.2723.
3
Cleavage of the cap binding protein complex polypeptide p220 is not effected by the second poliovirus protease 2A.帽结合蛋白复合体多肽p220的切割不受第二种脊髓灰质炎病毒蛋白酶2A的影响。
Virology. 1986 Apr 15;150(1):299-303. doi: 10.1016/0042-6822(86)90291-6.
4
Poliovirus proteinase 2A induces cleavage of eucaryotic initiation factor 4F polypeptide p220.脊髓灰质炎病毒蛋白酶2A诱导真核起始因子4F多肽p220的裂解。
J Virol. 1987 Sep;61(9):2711-8. doi: 10.1128/JVI.61.9.2711-2718.1987.
5
Proteolysis of the p220 component of the cap-binding protein complex is not sufficient for complete inhibition of host cell protein synthesis after poliovirus infection.脊髓灰质炎病毒感染后，帽结合蛋白复合体的p220组分的蛋白水解作用不足以完全抑制宿主细胞蛋白质合成。
J Virol. 1987 Apr;61(4):986-91. doi: 10.1128/JVI.61.4.986-991.1987.
6
Relationship of p220 cleavage during picornavirus infection to 2A proteinase sequencing.小核糖核酸病毒感染期间p220裂解与2A蛋白酶测序的关系。
J Virol. 1988 Nov;62(11):4216-23. doi: 10.1128/JVI.62.11.4216-4223.1988.
7
Cap-binding complex protein p220 is not cleaved during echovirus 22 replication in HeLa cells.帽结合复合蛋白p220在埃可病毒22于HeLa细胞中复制期间未被裂解。
J Virol. 1991 Jul;65(7):3903-5. doi: 10.1128/JVI.65.7.3903-3905.1991.
8
Variations in cap-binding complexes from uninfected and poliovirus-infected HeLa cells.未感染和脊髓灰质炎病毒感染的HeLa细胞中帽结合复合物的变化。
J Biol Chem. 1990 May 5;265(13):7492-500.
9
Leader protein of foot-and-mouth disease virus is required for cleavage of the p220 component of the cap-binding protein complex.口蹄疫病毒的前导蛋白是帽结合蛋白复合体p220组分裂解所必需的。
J Virol. 1988 Nov;62(11):4407-9. doi: 10.1128/JVI.62.11.4407-4409.1988.
10
Monoclonal antibody-aided characterization of cellular p220 in uninfected and poliovirus-infected HeLa cells: subcellular distribution and identification of conformers.单克隆抗体辅助鉴定未感染和脊髓灰质炎病毒感染的HeLa细胞中的细胞p220：亚细胞分布及构象体鉴定
J Virol. 1987 Sep;61(9):2702-10. doi: 10.1128/JVI.61.9.2702-2710.1987.

引用本文的文献

1
Poliovirus proteinase 2A induces cleavage of eucaryotic initiation factor 4F polypeptide p220.脊髓灰质炎病毒蛋白酶2A诱导真核起始因子4F多肽p220的裂解。
J Virol. 1987 Sep;61(9):2711-8. doi: 10.1128/JVI.61.9.2711-2718.1987.
2
Restriction of translation of capped mRNA in vitro as a model for poliovirus-induced inhibition of host cell protein synthesis: relationship to p220 cleavage.体外帽状mRNA翻译的限制作为脊髓灰质炎病毒诱导宿主细胞蛋白质合成抑制的模型：与p220裂解的关系。
J Virol. 1987 Aug;61(8):2480-8. doi: 10.1128/JVI.61.8.2480-2488.1987.
3
Proteolysis of the p220 component of the cap-binding protein complex is not sufficient for complete inhibition of host cell protein synthesis after poliovirus infection.

本文引用的文献

1
Production of antisera with small doses of immunogen: multiple intradermal injections.用小剂量免疫原制备抗血清：多次皮内注射。
Methods Enzymol. 1981;73(Pt B):46-52. doi: 10.1016/0076-6879(81)73055-6.
2
Inactivation of cap-binding proteins accompanies the shut-off of host protein synthesis by poliovirus.帽结合蛋白的失活伴随着脊髓灰质炎病毒对宿主蛋白质合成的关闭。
Proc Natl Acad Sci U S A. 1982 Jun;79(11):3447-51. doi: 10.1073/pnas.79.11.3447.
3
New initiation factor activity required for globin mRNA translation.珠蛋白mRNA翻译所需的新起始因子活性。
脊髓灰质炎病毒感染后，帽结合蛋白复合体的p220组分的蛋白水解作用不足以完全抑制宿主细胞蛋白质合成。
J Virol. 1987 Apr;61(4):986-91. doi: 10.1128/JVI.61.4.986-991.1987.
4
Regulation of protein synthesis in virus-infected animal cells.病毒感染动物细胞中蛋白质合成的调控。
Adv Virus Res. 1986;31:229-92. doi: 10.1016/s0065-3527(08)60265-1.
5
Poliovirus mutant that does not selectively inhibit host cell protein synthesis.不选择性抑制宿主细胞蛋白质合成的脊髓灰质炎病毒突变体。
Mol Cell Biol. 1985 Nov;5(11):2913-23. doi: 10.1128/mcb.5.11.2913-2923.1985.
6
Relationship of p220 cleavage during picornavirus infection to 2A proteinase sequencing.小核糖核酸病毒感染期间p220裂解与2A蛋白酶测序的关系。
J Virol. 1988 Nov;62(11):4216-23. doi: 10.1128/JVI.62.11.4216-4223.1988.
7
Degradation of cellular proteins during poliovirus infection: studies by two-dimensional gel electrophoresis.脊髓灰质炎病毒感染期间细胞蛋白质的降解：二维凝胶电泳研究
J Virol. 1989 Nov;63(11):4729-35. doi: 10.1128/JVI.63.11.4729-4735.1989.
8
Eukaryotic initiation factor 3 is required for poliovirus 2A protease-induced cleavage of the p220 component of eukaryotic initiation factor 4F.真核生物起始因子3是脊髓灰质炎病毒2A蛋白酶诱导真核生物起始因子4F的p220组分裂解所必需的。
Proc Natl Acad Sci U S A. 1990 Dec;87(24):9529-33. doi: 10.1073/pnas.87.24.9529.
9
Relationship of eukaryotic initiation factor 3 to poliovirus-induced p220 cleavage activity.真核起始因子3与脊髓灰质炎病毒诱导的p220切割活性的关系。
J Virol. 1992 May;66(5):2943-51. doi: 10.1128/JVI.66.5.2943-2951.1992.
J Biol Chem. 1983 May 10;258(9):5804-10.
4
Involvement of eukaryotic initiation factor 4A in the cap recognition process.真核生物起始因子4A在帽识别过程中的作用。
J Biol Chem. 1983 Sep 25;258(18):11398-403.
5
Inhibition of HeLa cell protein synthesis following poliovirus infection correlates with the proteolysis of a 220,000-dalton polypeptide associated with eucaryotic initiation factor 3 and a cap binding protein complex.脊髓灰质炎病毒感染后，HeLa细胞蛋白质合成的抑制与一种与真核起始因子3和帽结合蛋白复合物相关的220,000道尔顿多肽的蛋白水解有关。
J Biol Chem. 1982 Dec 25;257(24):14806-10.
6
Proteolytic processing of poliovirus polypeptides: antibodies to polypeptide P3-7c inhibit cleavage at glutamine-glycine pairs.脊髓灰质炎病毒多肽的蛋白水解加工：针对多肽P3-7c的抗体抑制谷氨酰胺-甘氨酸对处的切割。
Proc Natl Acad Sci U S A. 1982 Jul;79(13):3973-7. doi: 10.1073/pnas.79.13.3973.
7
Poliovirus-induced inhibition of host-cell protein synthesis.脊髓灰质炎病毒引起的宿主细胞蛋白质合成抑制。
Cell. 1982 Mar;28(3):435-6. doi: 10.1016/0092-8674(82)90195-7.
8
Two forms of purified m7G-cap binding protein with different effects on capped mRNA translation in extracts of uninfected and poliovirus-infected HeLa cells.两种纯化的m7G帽结合蛋白，对未感染和脊髓灰质炎病毒感染的HeLa细胞提取物中的加帽mRNA翻译有不同影响。
J Biol Chem. 1981 Aug 10;256(15):7691-4.
9
Functional characterization of eukaryotic mRNA cap binding protein complex: effects on translation of capped and naturally uncapped RNAs.真核生物mRNA帽结合蛋白复合体的功能特性：对带帽和天然无帽RNA翻译的影响
Biochemistry. 1984 May 22;23(11):2456-62. doi: 10.1021/bi00306a021.
10
Demonstration in vitro that eucaryotic initiation factor 3 is active but that a cap-binding protein complex is inactive in poliovirus-infected HeLa cells.体外实验证明，在脊髓灰质炎病毒感染的HeLa细胞中，真核起始因子3具有活性，但帽结合蛋白复合体无活性。
J Virol. 1984 Sep;51(3):832-7. doi: 10.1128/JVI.51.3.832-837.1984.