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首页> 外文期刊>Journal of Molecular Biology >Vitamin B12 stalls the 80 s ribosomal complex on the hepatitis C internal ribosome entry site.
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Vitamin B12 stalls the 80 s ribosomal complex on the hepatitis C internal ribosome entry site.

机译：维生素B12使80年代核糖体复合物停滞在丙型肝炎内部核糖体进入位点。

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摘要

The effect of cyanocobalamin (CNCbl, vitamin B12) on hepatitis C virus internal ribosome entry site (HCV IRES)-dependent initiation of translation was studied by ribosomal toeprinting and sucrose gradient centrifugation analysis. These results suggested that CNCbl did not inhibit HCV IRES-dependent translation by a competitive binding mechanism. CNCbl allowed 80 S elongation complex formation on the mRNA, but stalled the initiation at that point, effectively trapping the 80 S ribosomal complexes on the HCV IRES. CNCbl had no effect on cap-dependent mRNA, consistent with the known mRNA specificity of this translational inhibitor. To help elucidate the mechanism, comparative data were collected for the well-characterised translation inhibitors cycloheximide and 5'-guanylyl-imidophosphate. Although CNCbl stalled HCV IRES-dependent translation at approximately the same step in initiation as cycloheximide, the mechanisms of these two inhibitors are distinct. (c) 2002 Elsevier Science Ltd.
机译：通过核糖体印迹和蔗糖梯度离心分析，研究了氰钴胺素（CNCbl，维生素B12）对丙型肝炎病毒内部核糖体进入位点（HCV IRES）依赖性翻译起始的影响。这些结果表明CNCbl1没有通过竞争性结合机制抑制HCV IRES依赖性翻译。 CNCbl允许在mRNA上形成80 S延伸复合物，但在这一点停止了起始，有效地将80 S核糖体复合物捕获在HCV IRES上。 CNCb1对帽依赖性mRNA没有影响，与这种翻译抑制剂的已知mRNA特异性一致。为帮助阐明机理，收集了特征明确的翻译抑制剂环己酰亚胺和5'-胍基-亚氨基磷酸酯的比较数据。尽管CNCb1在与环己酰亚胺大致相同的起始步骤中停止了HCV IRES依赖性翻译，但这两种抑制剂的机制却截然不同。 （c）2002爱思唯尔科学有限公司

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