ArticleJournal of virology1999
Targeting of the visna virus tat protein to AP-1 sites: interactions with the bZIP domains of fos and jun in vitro and in vivo.
Article in Journal of virology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 23 citations in OpenAlex.
- Comparative Analysis of Tat-Dependent and Tat-Deficient Natural Lentiviruses.Veterinary sciences · 2015Review
- Review
- The AP-1 binding sites located in the pol gene intragenic regulatory region of HIV-1 are important for viral replication.PloS one · 2011Article
- Genomic characterization of a slow/low maedi visna virus.Virus genes · 2004Article
- Feline immunodeficiency virus OrfA is distinct from other lentivirus transactivators.Journal of virology · 2002Article
- Visna virus-induced activation of MAPK is required for virus replication and correlates with virus-induced neuropathology.Journal of virology · 2002Article
- Construction and in vitro characterization of attenuated feline immunodeficiency virus long terminal repeat mutant viruses.Journal of virology · 2001Article
- Human immunodeficiency virus and AIDS: insights from animal lentiviruses.Journal of virology · 2000Review
- Functional differences between human and bovine immunodeficiency virus Tat transcription factors.Journal of virology · 2000Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The visna virus Tat protein is required for efficient viral transcription from the visna virus long terminal repeat (LTR). AP-1 sites within the visna virus LTR, which can be bound by the cellular transcription factors Fos and Jun, are also necessary for Tat-mediated transcriptional activation. A potential mechanism by which the visna virus Tat protein could target the viral promoter is by protein-protein interactions with Fos and/or Jun bound to AP-1 sites in the visna virus LTR. Once targeted to the visna virus promoter, the Tat protein could then interact with basal transcription factors to activate transcription. To examine protein-protein interactions with cellular proteins at the visna virus promoter, we used an in vitro protein affinity chromatography assay and electrophoretic mobility shift assay, in addition to an in vivo two-hybrid assay, to show that the visna virus Tat protein specifically interacts with the cellular transcription factors Fos and Jun and the basal transcription factor TBP (TATA binding protein). The Tat domain responsible for interactions with Fos and Jun was localized to an alpha-helical domain within amino acids 34 to 69 of the protein. The TBP binding domain was localized to amino acids 1 to 38 of Tat, a region previously described by our laboratory as the visna virus Tat activation domain. The bZIP domains of Fos and Jun were found to be important for the interactions with Tat. Mutations within the basic domains of Fos and Jun abrogated binding to Tat in the in vitro assays. The visna virus Tat protein was also able to interact with covalently cross-linked Fos and Jun dimers. Thus, the visna virus Tat protein appears to target AP-1 sites in the viral promoter in a mechanism similar to the interaction of human T-cell leukemia virus type 1 Tax with the cellular transcription factor CREB, by binding the basic domains of an intact bZIP dimer. The association between Tat, Fos, and Jun would position Tat proximal to the viral TATA box, where the visna virus Tat activation domain could contact TBP to activate viral transcription.
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