Does HIV-1 Tat induce a change in viral initiation rights?
Article Abstract:
HIV-1 Tat protein activates viral mRNA transcription at the level of transcript initiation. This sugggests that the mechanism of action of Tat might resemble many other transcriptional regulatory proteins. However, Tat remains unique in that its target is an RNA, rather than a DNA, sequence. It acts on a promoter element that is already transcriptionally active. Furthermore, RNA-mediated transcriptional activation might facilitate not only the rapid induction of transcription from the HIV-1 LTR but also, potentially, subsequent down-regulation of viral mRNA synthesis.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1993
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HIV-1 auxiliary proteins: making connections in a dying cell
Article Abstract:
The genomic organization of HIV-1 is more complex compared to other human retroviruses such as encogenic murine and avian viruses because this HIV virus can express six new additional small proteins which are termed as Tat, Rev, Vif, Nef, Vpr and Vpu. The Tat and Rev proteins are necessary in HIV replication while the Vif protein is critical in various culture settings such as the human lymphocytes. The Nef, Vpr and Vpu have modest phenotypes in cell culture assays. These auxiliary proteins may have more important roles in the cycle of HIV replication.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1998
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Identification of a novel cellular cofactor for the Rev/Rex class of retroviral regulatory proteins
Article Abstract:
HIV-1 Rev is the prototype of a group of retroviral regulatory proteins that cause of sequence-specific nuclear export of target RNAs. The Rev/Rex activation domain-binding (Rab) is the activation domain-specific cofactor for the Rev/Rex class of RNA export factors. The Rab protein occupies a binding site on HIV-1 Rev that clearly matches that predicted by genetic analysis. Rab binds the Rev activation domain when Rev is assembled on to its RNA target and can enhance Rev activity when overexpressed.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1995
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