病毒的技巧

Science's STKE Pub Date : 2002-08-06 DOI:10.1126/scisignal.1442002tw290

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摘要

疱疹病毒在宿主细胞核内复制，但形成的颗粒太大，无法通过核孔。它们是如何逃脱的?Muranyi等人(见Sanchez和Spector的观点)发现，小鼠巨细胞病毒破坏细胞蛋白质的正常活动，以帮助其逃逸。一对病毒蛋白(M50/p35和M53/p38)在核膜上形成病毒衣壳的“对接站”。然后M50/p35招募细胞蛋白激酶C磷酸化并分解核层的丝状蛋白网络。陈晓明，陈晓明，陈晓明，陈晓明。细胞激酶的克隆及其在细胞内的应用，中国生物医学工程学报，2002,33(4):557 - 557。[摘要]V. Sanchez, d.h. Spector，巨细胞病毒的适时退出，科学29(7)，778-779(2002)。【摘要】【全文】

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Viral Tricks

Herpesviruses replicate in the nucleus of host cells, but the particles formed are too big to pass through nuclear pores. How do they escape? Muranyi et al. (see the Perspective by Sanchez and Spector) found that murine cytomegalovirus subverts the normal activity of a cellular protein to aid its escape. A pair of viral proteins (M50/p35 and M53/p38) form a "docking station" for the viral capsids on the inner nuclear membrane. M50/p35 then recruits cellular protein kinase C to phosphorylate and disassemble the filamentous protein network of the nuclear lamina. W. Muranyi, J. Haas, M. Wagner, G. Krohne, U. H. Koszinowski, Cytomegalovirus recruitment of cellular kinases to dissolve the nuclear lamina, Science 297, 854-857 (2002). [Abstract] [Full Text] V. Sanchez, D. H. Spector, CMV makes a timely exit, Science 297, 778-779 (2002). [Summary] [Full Text]

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