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首页> 外文期刊>Virology >Significance of the YLDL motif in the M protein and Alix/AIP1 for Sendai virus budding in the context of virus infection.
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Significance of the YLDL motif in the M protein and Alix/AIP1 for Sendai virus budding in the context of virus infection.

机译:在病毒感染的背景下,M蛋白和Alix / AIP1中的YLDL基序对于仙台病毒出芽的意义。

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Sendai virus (SeV) M protein has a YLDL motif, which is essential for budding of virus-like particles (VLPs) by expression of the M protein. We investigated the importance of the YLDL motif for SeV budding. Virus budding of an M-deficient SeV was not rescued by transient expression of motif mutants, M-A2 (ALDA) and M-A4 (AAAA), and viruses possessing those mutations hardly propagated in cultured cells. However, a budding-competent revertant virus, SeV M-A2R, was obtained from SeV M-A2, and nucleotide sequencing showed an ALDV sequence at the motif instead of the ALDA sequence derived from M-A2. The M-A2R protein rescued budding of an M-deficient SeV, formed VLPs when expressed with viral C protein, and restored the capacity to bind with Alix/AIP1. The results indicate that the YLDL motif is essential for efficient budding in the context of virus infection and suggest involvement of Alix/AIP1 in SeV budding.
机译:仙台病毒(SeV)M蛋白具有YLDL基序,该基序对于通过表达M蛋白表达病毒样颗粒(VLP)是必不可少的。我们调查了YLDL基序对于SeV出芽的重要性。 M缺陷型SeV的病毒出芽不能通过基序突变体M-A2(ALDA)和M-A4(AAAA)的瞬时表达来挽救,具有这些突变的病毒几乎不会在培养细胞中繁殖。然而,从SeV M-A2获得了具有芽芽能力的逆转录病毒SeV M-A2R,核苷酸测序显示在基序上有一个ALDV序列,而不是衍生自M-A2的ALDA序列。 M-A2R蛋白挽救了M缺陷型SeV的出芽,当与病毒C蛋白一起表达时形成VLP,并恢复了与Alix / AIP1结合的能力。结果表明,在病毒感染的情况下,YLDL基序对于有效出芽是必不可少的,并表明Alix / AIP1参与了SeV出芽。

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