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      The structure and function of the rous sarcoma virus RNA stability element.

      1 ,
      Journal of cellular biochemistry
      Wiley-Blackwell

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          Abstract

          For simple retroviruses, such as the Rous sarcoma virus (RSV), post-transcriptional control elements regulate viral RNA splicing, export, stability, and packaging into virions. These RNA sequences interact with cellular host proteins to regulate and facilitate productive viral infections. One such element, known as the RSV stability element (RSE), is required for maintaining stability of the full-length unspliced RNA. This viral RNA serves as the mRNA for the Gag and Pol proteins and also as the genome packaged in progeny virions. When the RSE is deleted from the viral RNA, the unspliced RNA becomes unstable and is degraded in a Upf1-dependent manner. Current evidence suggests that the RSE inhibits recognition of the viral gag termination codon by the nonsense-mediated mRNA decay (NMD) pathway. We believe that the RSE acts as an insulator to NMD, thereby preventing at least one of the required functional steps that target an mRNA for degradation. Here, we discuss the history of the RSE and the current model of how the RSE is interacting with cellular NMD factors.

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          Author and article information

          Journal
          J. Cell. Biochem.
          Journal of cellular biochemistry
          Wiley-Blackwell
          1097-4644
          0730-2312
          Nov 2011
          : 112
          : 11
          Affiliations
          [1 ] Department of Biology, The Johns Hopkins University, 3400 N. Charles St., Baltimore, Maryland 21218, USA.
          Article
          NIHMS499126
          10.1002/jcb.23272
          3810391
          21769913
          ee52ea93-f97a-4f95-9977-1b996dc26581
          History

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