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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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A nuclear translational block imposed by the HIV-1 U3 region is relieved by the Tat-TAR interaction.

Replication of HIV-1 depends on the viral Tat protein, which functions via a target sequence, TAR, present in the proviral long terminal repeat (LTR) and at the 5' end of viral mRNAs. We have shown that Tat potentiates the expression of TAR-containing RNAs, but only when Tat and the TAR-containing RNA are present in the nucleus. We now show that a small change in the TAR loop abolishes nuclear potentiation by Tat. Furthermore, the HIV-1 U3 region induces expression incompetence in mRNA synthesized by this promoter. RNAs of identical structure are, however, translated efficiently when produced from the CMV-IE promoter. The Tat-TAR system appears, therefore, to rescue the expression potential of HIV-1 LTR-directed RNA.[1]

References

  1. A nuclear translational block imposed by the HIV-1 U3 region is relieved by the Tat-TAR interaction. Braddock, M., Thorburn, A.M., Chambers, A., Elliott, G.D., Anderson, G.J., Kingsman, A.J., Kingsman, S.M. Cell (1990) [Pubmed]
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