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核苷对葡萄糖剥夺的L929细胞耐热性的恢复及葡萄糖调节蛋白合成的抑制作用。

Nucleoside restoration of heat resistance and suppression of glucose-regulated protein synthesis by glucose-deprived L929 cells.

作者信息

Lanks K W, Gao J P, Kasambalides E J

机构信息

Department of Pathology, SUNY Health Science Center, Brooklyn 11203.

出版信息

Cancer Res. 1988 Mar 15;48(6):1442-5.

PMID:3345514
Abstract

Depriving cultured cells of glucose increases glucose-regulated protein synthesis, suppresses heat shock protein synthesis, and increases sensitivity to killing by hyperthermia. The present study shows that supplementation of glucose-free culture medium with uridine or a number of other nucleosides reverses all these effects of glucose deprivation. Uridine is more effective in this regard than equimolar concentrations of glucose, and ribose is relatively ineffective. Uridine does not suppress glucose-regulated protein synthesis that has been induced by glycosylation inhibitors, calcium chelation, or anoxia. We infer from these data that the effects of glucose deprivation may result from inhibition of ribonucleoside synthesis and that ribonucleosides may be directly involved in regulating glucose-regulated protein and heat shock protein synthesis as well as in protecting cells against hyperthermic cytotoxicity.

摘要

剥夺培养细胞的葡萄糖会增加葡萄糖调节蛋白的合成,抑制热休克蛋白的合成,并增加细胞对热疗杀伤的敏感性。本研究表明,在无葡萄糖的培养基中添加尿苷或其他多种核苷可逆转葡萄糖剥夺的所有这些效应。在这方面,尿苷比等摩尔浓度的葡萄糖更有效,而核糖相对无效。尿苷不会抑制由糖基化抑制剂、钙螯合或缺氧诱导的葡萄糖调节蛋白的合成。我们从这些数据推断,葡萄糖剥夺的效应可能是由于核糖核苷合成受到抑制,并且核糖核苷可能直接参与调节葡萄糖调节蛋白和热休克蛋白的合成,以及保护细胞免受热疗细胞毒性的影响。

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