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本文引用的文献

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Genes of variola and vaccinia viruses necessary to overcome the host protective mechanisms.天花病毒和牛痘病毒中克服宿主保护机制所必需的基因。
FEBS Lett. 1993 Mar 15;319(1-2):80-3. doi: 10.1016/0014-5793(93)80041-r.
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Nuclear localization of a double-stranded RNA-binding protein encoded by the vaccinia virus E3L gene.痘苗病毒E3L基因编码的双链RNA结合蛋白的核定位
Virology. 1993 Aug;195(2):732-44. doi: 10.1006/viro.1993.1424.
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Recombinant vaccinia virus K3L gene product prevents activation of double-stranded RNA-dependent, initiation factor 2 alpha-specific protein kinase.重组痘苗病毒K3L基因产物可阻止双链RNA依赖性起始因子2α特异性蛋白激酶的激活。
J Biol Chem. 1993 Jun 15;268(17):12837-42.
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Identification of a conserved motif that is necessary for binding of the vaccinia virus E3L gene products to double-stranded RNA.鉴定一种保守基序,该基序是痘苗病毒E3L基因产物与双链RNA结合所必需的。
Virology. 1993 Jun;194(2):537-47. doi: 10.1006/viro.1993.1292.
5
The E3L and K3L vaccinia virus gene products stimulate translation through inhibition of the double-stranded RNA-dependent protein kinase by different mechanisms.E3L和K3L痘苗病毒基因产物通过不同机制抑制双链RNA依赖性蛋白激酶来刺激翻译。
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The mouse antiphosphotyrosine immunoreactive kinase, TIK, is indistinguishable from the double-stranded RNA-dependent, interferon-induced protein kinase, PKR.小鼠抗磷酸酪氨酸免疫反应性激酶TIK与双链RNA依赖性干扰素诱导蛋白激酶PKR无法区分。
Nucleic Acids Res. 1993 Oct 11;21(20):4830-5. doi: 10.1093/nar/21.20.4830.
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Reversal of the interferon-sensitive phenotype of a vaccinia virus lacking E3L by expression of the reovirus S4 gene.通过呼肠孤病毒S4基因的表达逆转缺乏E3L的痘苗病毒的干扰素敏感表型。
J Virol. 1995 Jan;69(1):499-505. doi: 10.1128/JVI.69.1.499-505.1995.
8
TAR RNA-binding protein is an inhibitor of the interferon-induced protein kinase PKR.TAR RNA结合蛋白是干扰素诱导蛋白激酶PKR的一种抑制剂。
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Products of the porcine group C rotavirus NSP3 gene bind specifically to double-stranded RNA and inhibit activation of the interferon-induced protein kinase PKR.猪C组轮状病毒NSP3基因产物特异性结合双链RNA并抑制干扰素诱导蛋白激酶PKR的激活。
J Virol. 1994 Jun;68(6):3821-9. doi: 10.1128/JVI.68.6.3821-3829.1994.
10
Vaccinia rescue of VSV from interferon-induced resistance: reversal of translation block and inhibition of protein kinase activity.痘苗病毒从干扰素诱导的抗性中拯救水疱性口炎病毒:翻译阻断的逆转和蛋白激酶活性的抑制
Virology. 1983 Nov;131(1):128-36. doi: 10.1016/0042-6822(83)90539-1.

通过E3L突变体拯救缺失E3L基因的痘苗病毒。

Rescue of vaccinia virus lacking the E3L gene by mutants of E3L.

作者信息

Chang H W, Uribe L H, Jacobs B L

机构信息

Department of Microbiology, Arizona State University, Tempe 85287-2701, USA.

出版信息

J Virol. 1995 Oct;69(10):6605-8. doi: 10.1128/JVI.69.10.6605-6608.1995.

DOI:10.1128/JVI.69.10.6605-6608.1995
PMID:7666567
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC189568/
Abstract

Vaccinia virus with the E3L gene deleted was able to replicate in RK-13 but not HeLa cells. This host range phenotype could be complemented by an E3L gene expressed transiently from a plasmid. Analysis of mutants of E3L indicates that the ability to complement deletion of E3L correlates with the ability of mutated proteins to bind double-stranded RNA but not with their ability to migrate to the nucleus.

摘要

缺失E3L基因的痘苗病毒能够在RK - 13细胞中复制,但不能在HeLa细胞中复制。这种宿主范围表型可以通过从质粒瞬时表达的E3L基因来互补。对E3L突变体的分析表明,互补E3L缺失的能力与突变蛋白结合双链RNA的能力相关,而与其迁移到细胞核的能力无关。