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The toxicity of 9-beta-D-arabinofuranosyladenine to purine-requiring Escherichia coli.9-β-D-阿拉伯呋喃糖基腺嘌呤对需要嘌呤的大肠杆菌的毒性。
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9-BETA-D-ARABINOFURANOSYLADENINE AS AN INHIBITOR OF METABOLISM IN NORMAL AND NEOPLASTIC CELLS.9-β-D-阿拉伯呋喃糖基腺嘌呤作为正常细胞和肿瘤细胞代谢的抑制剂
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Antiviral activity of 9-beta-D-arabinofuranosyladenine. I. Cell culture studies.9-β-D-阿拉伯呋喃糖基腺嘌呤的抗病毒活性。I. 细胞培养研究。
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Studies on the biosynthesis and role of diguanosine tetraphosphate during growth and development of Artemia salina.
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Ribonucleic acid synthesis of vesicular stomatitis virus, II. An RNA polymerase in the virion.水泡性口炎病毒的核糖核酸合成,II。病毒粒子中的一种RNA聚合酶。
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Effects of trypsin on replication of parainfluenza-3 virus in HEp-2 cell cultures.胰蛋白酶对副流感3型病毒在人喉表皮样癌细胞(HEp-2)培养物中复制的影响。
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The antiviral activity of 9-beta-D-arabinofuranosyladenine (ARA-A).9-β-D-阿拉伯呋喃糖基腺嘌呤(阿糖腺苷,ARA-A)的抗病毒活性。
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9-β-D-阿拉伯呋喃糖基腺嘌呤对水疱性口炎病毒复制的抑制作用

Inhibition of vesicular stomatitis virus replication by 9-beta-D-arabinofuranosyladenine.

作者信息

Grant J A, Sabina L R

出版信息

Antimicrob Agents Chemother. 1972 Sep;2(3):201-5. doi: 10.1128/AAC.2.3.201.

DOI:10.1128/AAC.2.3.201
PMID:4364172
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC444291/
Abstract

9-beta-d-Arabinofuranosyladenine (Ara-A) effectively inhibited the production of infectious vesicular stomatitis virus (VSV) in MDBK cells. Furthermore, inhibition was shown to begin as early as the first 3 hr of infection. Studies employing (3)H-l-leucine indicated that Ara-A did not affect protein synthesis in uninfected cells, although it did cause a marked stimulation of protein synthesis in VSV-infected cells during the log phase of the growth cycle. Puromycin, an inhibitor of protein synthesis, was a more effective viral inhibitor than Ara-A. However, the combination of Ara-A and puromycin was less effective than puromycin alone except when present for long time periods. Short-term labeling experiments with (3)H-uridine demonstrated that Ara-A depressed ribonucleic acid (RNA) synthesis in uninfected cells, whereas periods of stimulation and depression of radioisotope incorporation occurred in infected cells. The results support the notion that Ara-A is incorporated into RNA early during viral replication.

摘要

9-β-D-阿拉伯呋喃糖基腺嘌呤(Ara-A)可有效抑制水泡性口炎病毒(VSV)在MDBK细胞中的产生。此外,研究表明抑制作用最早在感染后的前3小时就开始了。使用³H-L-亮氨酸的研究表明,Ara-A对未感染细胞的蛋白质合成没有影响,尽管它在生长周期的对数期确实会显著刺激VSV感染细胞中的蛋白质合成。蛋白质合成抑制剂嘌呤霉素是比Ara-A更有效的病毒抑制剂。然而,Ara-A和嘌呤霉素的组合比单独使用嘌呤霉素效果更差,除非长时间存在。用³H-尿苷进行的短期标记实验表明,Ara-A可抑制未感染细胞中的核糖核酸(RNA)合成,而在感染细胞中则会出现放射性同位素掺入的刺激和抑制期。这些结果支持了Ara-A在病毒复制早期被掺入RNA的观点。