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对痘苗病毒感染的热休克反应

Heat shock response to vaccinia virus infection.

作者信息

Sedger L, Ruby J

机构信息

Division of Cell Biology, John Curtin School of Medical Research, Australian National University, Canberra.

出版信息

J Virol. 1994 Jul;68(7):4685-9. doi: 10.1128/JVI.68.7.4685-4689.1994.

Abstract

We have investigated the induction of heat shock proteins (HSPs) in mice infected with vaccinia virus. Vaccinia virus replicates to high levels in the ovaries of infected mice and causes a significant inhibition of host cell DNA, RNA, and protein synthesis. Many HSPs are constitutively expressed in murine ovarian tissue at low levels, consistent with their obligatory role in normal physiological events. In contrast with these events, HSP expression was augmented in virus-infected mouse ovaries 6 days postinfection. In particular, there was a dramatic increase in the expression of a protein identified as the inducible 72-kDa HSP. Analysis of cellular mRNA confirmed this protein to be the major mouse inducible HSP70 and demonstrated its presence within virus-infected cells. Hence, we have demonstrated the expression of stress proteins during poxvirus infection in vivo.

摘要

我们研究了感染痘苗病毒的小鼠体内热休克蛋白(HSPs)的诱导情况。痘苗病毒在感染小鼠的卵巢中大量复制,并显著抑制宿主细胞的DNA、RNA和蛋白质合成。许多热休克蛋白在小鼠卵巢组织中以低水平组成性表达,这与其在正常生理事件中的重要作用相一致。与这些情况相反,感染病毒后6天,热休克蛋白的表达在病毒感染的小鼠卵巢中增强。特别是,一种被鉴定为诱导型72 kDa热休克蛋白的蛋白质表达急剧增加。对细胞mRNA的分析证实该蛋白是主要的小鼠诱导型热休克蛋白70,并证明其存在于病毒感染的细胞内。因此,我们证明了体内痘病毒感染期间应激蛋白的表达。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f875/236399/e3f2a64699ad/jvirol00016-0590-a.jpg

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