Anti-termination of transcription within the long terminal repeat of HIV-1 by tat gene product

  title={Anti-termination of transcription within the long terminal repeat of HIV-1 by tat gene product},
  author={Shaw-yi Kao and Andrew F. Calman and Paul A. Luciw and B Matija Peterlin},
Human immunodeficiency virus-1 (HIV-1) gene expression is controlled by cellular transcription factors and by virally encoded trans-activation proteins of the HIV-1 tat and art/trs genes, which are essential for viral replication1,9–11. Tat trans-activates HIV-1 gene expression by interacting with the trans-acting response element (TAR) located within the HIV-1 long terminal repeat (LTR) (ref. 2). In transient expression assays, tat mediates its effects largely by increasing the steady-state… 
Activation of transcription by HIV-1 Tat protein tethered to nascent RNA through another protein
It is concluded that activation of transcription by Tat can occur by direct binding to nascent RNA, and that the sole function of TAR may be to provide a Tat-binding site, which suggests that cellular proteins that bind specifically to TAR RNA or TAR DNA may not be essential for Tat-responsiveness.
Specific binding of RNA polymerase II to the human immunodeficiency virus trans-activating region RNA is regulated by cellular cofactors and Tat.
The results suggest that Tat may function to alter RNA polymerase II, which is paused due to its binding to HIV-1 TAR RNA with resultant stimulation of its transcriptional elongation properties.
Tat and the HIV-1 promoter: A model for RNA-mediated regulation of transcription
The mechanism of trans-activation by Tat (including the role of TAR RNA) as well as the influence of host cell DNAbinding proteins on the assembly of productive and abortive transcription complexes at the HIV-1 promoter are considered.
Transcriptional but not translational regulation of HIV-1 by the tat gene product
An efficient adenovirus system for delivering the HIV-1 LTR attached to a reporter gene (chloramphenicol acetyltransferase; CAT) into cells and monitoring its activity is established, which responds to trans-activation in a HeLa cell line constitutively expressing the tat protein.
HIV-1 tat trans-activation requires the loop sequence within tar
The results of nucleotide substitution experiments are presented which suggest that tat trans-activation requires presentation of the sequence +30CUGGG+34 in tar within the loop of a RNA hairpin structure.
Trans-activation by HIV-1 Tat via a heterologous RNA binding protein
It is suggested that trans-activation by Tat can occur independently of TAR RNA and DNA binding proteins and that Tat exerts its effects on HIV-1 transcription by directly interacting with the TARRNA stem-loop.
Human-Specific Factors are Required for Tat-Mediated Trans-Activation of the HIV-1 and HIV-2 LTRs
HIV-1 Tat mediates its effect through a sequence termed TAR, which has been genetically defined to reside in the R region of the LTR (19).
HIV-1: Control of gene expression by the viral regulatory proteins Tat and Rev
This chapter reviews the roles of these regulatory proteins in the viral life-cycle, as well as structures and functions of Tat and Rev and their target sequences TAR and RRE.
Transcriptional elongation by purified RNA polymerase II is blocked at the trans-activation-responsive region of human immunodeficiency virus type 1 in vitro
The existence of this signal in the TAR stem-loop suggests that in vivo an antiattenuation factor, probably Tat, alone or in combination with other factors, acts to relieve the elongation block at the HIV-1 attenuation site.
Expression of an RNA glycosidase inhibits HIV-1 transactivation of transcription.
The primary effect of PAP on HIV-1 transcription is to reduce viral RNA synthesis by decreasing the abundance of Tat, providing a mechanistic explanation for the observed decrease in viral RNAs in cells expressing PAP.