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浅蓝菌素可阻断糖蛋白的脂肪酸酰化作用,并抑制水疱性口炎病毒和辛德毕斯病毒颗粒的形成。

Cerulenin blocks fatty acid acylation of glycoproteins and inhibits vesicular stomatitis and Sindbis virus particle formation.

作者信息

Schlesinger M J, Malfer C

出版信息

J Biol Chem. 1982 Sep 10;257(17):9887-90.

PMID:6286658
Abstract

Cerulenin, an antibiotic that inhibits de novo fatty acid and cholesterol biosynthesis, effectively inhibited the formation and release of virus particles from chicken embryo fibroblasts infected with Sindbis or vesicular stomatitis virus (VSV). When added for 1 h at 3 h postinfection, the antibiotic blocked VSV particle production by 80 to 90% and inhibited incorporation of [3H]palmitic acid into the VSV glycoprotein by an equivalent amount. The effect of this antibiotic on virus protein and RNA biosynthesis was significantly less than that on fatty acid acylation. Nonacylated virus glycoproteins accumulated inside and on the surface of cerulenin-treated cells. These data indicate that fatty acid acylation is not essential for intracellular transport of these membrane proteins, but it may have an important role in the interaction of glycoproteins with membranes during virus assembly and budding.

摘要

浅蓝菌素是一种抑制脂肪酸和胆固醇从头生物合成的抗生素,它能有效抑制感染辛德毕斯病毒或水疱性口炎病毒(VSV)的鸡胚成纤维细胞中病毒颗粒的形成和释放。在感染后3小时添加该抗生素1小时,它可使VSV颗粒产量减少80%至90%,并等量抑制[3H]棕榈酸掺入VSV糖蛋白。这种抗生素对病毒蛋白质和RNA生物合成的影响明显小于对脂肪酸酰化的影响。未酰化的病毒糖蛋白在经浅蓝菌素处理的细胞内和细胞表面积累。这些数据表明,脂肪酸酰化对于这些膜蛋白的细胞内运输并非必不可少,但它可能在病毒组装和出芽过程中糖蛋白与膜的相互作用中发挥重要作用。

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