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持续感染副粘病毒的C6大鼠胶质瘤细胞中磷脂甲基化的改变及信号转导受损。

Alteration in phospholipid methylation and impairment of signal transmission in persistently paramyxovirus-infected C6 rat glioma cells.

作者信息

Münzel P, Koschel K

出版信息

Proc Natl Acad Sci U S A. 1982 Jun;79(12):3692-6. doi: 10.1073/pnas.79.12.3692.

Abstract

The paramyxoviruses measles (subacute sclerosing panencephalitis, SSPE) virus and canine distemper virus (CDV) cause an impairment of the catecholamine-induced beta-adrenergic receptor-dependent cAMP generation in persistently infected C6 rat glioma cells. In C6 cells persistently infected with CDV the number of receptors is greatly reduced. Hirata and Axelrod have shown that the number of beta-adrenergic receptors could be regulated by methylation of phosphatidylethanolamine, resulting in lecithin synthesis [Hirata, F. & Axelrod, J. (1980) Science 209, 1082-1090]. We have therefore studied the methylation of phosphatidylethanolamine in persistently infected cells by the incorporation of [3H]methyl groups from [methyl-3H]methionine into phosphatidylethanolamine. In both infected systems, C6/ SSPE and C6/CDV, we observed a total loss of catecholamine-stimulated beta-adrenergic receptor-dependent methylation, whereas the beta-receptor-independent methylation of phospholipids was unchanged.

摘要

副粘病毒麻疹(亚急性硬化性全脑炎,SSPE)病毒和犬瘟热病毒(CDV)在持续感染的C6大鼠胶质瘤细胞中会损害儿茶酚胺诱导的β-肾上腺素能受体依赖性环磷酸腺苷(cAMP)的生成。在持续感染CDV的C6细胞中,受体数量大幅减少。平田和阿克塞尔罗德已经表明,β-肾上腺素能受体的数量可通过磷脂酰乙醇胺的甲基化来调节,从而导致卵磷脂的合成[平田,F. & 阿克塞尔罗德,J.(1980年)《科学》209,1082 - 1090]。因此,我们通过将[甲基 - ³H]甲硫氨酸中的[³H]甲基掺入磷脂酰乙醇胺,研究了持续感染细胞中磷脂酰乙醇胺的甲基化情况。在两个感染系统,即C6/SSPE和C6/CDV中,我们观察到儿茶酚胺刺激的β-肾上腺素能受体依赖性甲基化完全丧失,而磷脂的β受体非依赖性甲基化未发生变化。

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