Plagemann P G, Shea M A
J Virol. 1971 Jan;7(1):137-43. doi: 10.1128/JVI.7.1.137-143.1971.
The incorporation of uridine into the nucleotide pool of actinomycin-treated, mengovirus-infected Novikoff rat hepatoma cells in culture follows simple Michaelis-Menten kinetics, and the apparent V(max) and K(m) values are similar to those for uridine transport by uninfected cells. Incorporation of uridine into mengovirus-specific ribonucleic acid (RNA) also follows Michaelis-Menten kinetics, and the apparent K(m) (about 10 mum) is approximately the same as for uridine transport. Inhibition of uridine transport by the presence of adenosine, persantin, or phenethyl alcohol inhibits simultaneously and to the same extent the incorporation of uridine into the nucleotide pool and into viral RNA, without affecting viral RNA synthesis per se. Phenethyl alcohol, however, also inhibits virus maturation. The inhibition of uridine incorporation into the nucleotide pool and into viral RNA is of the simple competitive type, indicating that transport into the cells is the rate-limiting step in the incorporation of uridine into mengovirus RNA. The results also indicate that treatment with actinomycin D or mengovirus infection does not affect uridine transport.
在培养的经放线菌素处理、感染脑心肌炎病毒的诺维科夫大鼠肝癌细胞中,尿苷掺入核苷酸池遵循简单的米氏动力学,表观V(max)和K(m)值与未感染细胞的尿苷转运值相似。尿苷掺入脑心肌炎病毒特异性核糖核酸(RNA)也遵循米氏动力学,表观K(m)(约10μM)与尿苷转运的K(m)大致相同。腺苷、潘生丁或苯乙醇的存在对尿苷转运的抑制同时且同等程度地抑制了尿苷掺入核苷酸池和病毒RNA,而不影响病毒RNA本身的合成。然而,苯乙醇也抑制病毒成熟。尿苷掺入核苷酸池和病毒RNA的抑制是简单的竞争类型,表明转运进入细胞是尿苷掺入脑心肌炎病毒RNA的限速步骤。结果还表明,用放线菌素D处理或感染脑心肌炎病毒不影响尿苷转运。