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首页> 外文期刊>Cellular immunology >Amino acid at position 176 was essential for porcine reproductive and respiratory syndrome virus (PRRSV) non-structural protein 1 alpha (nsp1 alpha) as an inhibitor to the induction of IFN-beta
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Amino acid at position 176 was essential for porcine reproductive and respiratory syndrome virus (PRRSV) non-structural protein 1 alpha (nsp1 alpha) as an inhibitor to the induction of IFN-beta

机译:176位氨基酸对于猪繁殖与呼吸综合征病毒(PRRSV)非结构蛋白1 alpha(nsp1 alpha)是必需的,可作为诱导IFN-β的抑制剂

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Previous studies have shown that porcine reproductive and respiratory syndrome virus (PRRSV) non-structural protein 1 alpha (nsp1 alpha) was the interferon (IFN) antagonist. However, the mechanism was unclear. In the present study, deletion of the carboxyl-terminal extension (CTE) (167-180 amino acid (aa)) made nsp1 alpha lose its inhibitory ability to the induction of IFN-beta. And a series of C-terminal truncated mutants for nsp1 alpha showed that 1-176 aa of nsp1 alpha was able to inhibit the induction of IFN-beta and deleting or mutating the amino acid F176 made nsp1 alpha not inhibit the induction of IFN-beta. In conclusion, the CTE and the amino acid F176 were critical for nsp1 alpha as the IFN antagonist and the region representing 167-176 was the minimal subunit of the CTE for nsp1 alpha to retain its suppressive activity to the induction of IFN-beta. (C) 2012 Published by Elsevier Inc.
机译:先前的研究表明,猪生殖和呼吸综合症病毒(PRRSV)非结构蛋白1α(nsp1 alpha)是干扰素(IFN)拮抗剂。但是,机制尚不清楚。在本研究中,羧基末端延伸(CTE)(167-180个氨基酸(aa))的缺失使nsp1α失去了其对IFN-β诱导的抑制能力。并且一系列针对nsp1 alpha的C末端截短突变体表明,nsp1 alpha的1-176aa能够抑制IFN-beta的诱导,缺失或突变使nsp1 alpha的氨基酸F176不能抑制IFN-beta的诱导。总之,CTE和氨基酸F176对于nsp1α作为IFN拮抗剂至关重要,而代表167-176的区域是nsp1 alpha的CTE的最小亚基,以保持其对IFN-β诱导的抑制活性。 (C)2012由Elsevier Inc.出版

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