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Transcription factor PRDII-BF1 activates human immunodeficiency virus type 1 gene expression
J S Seeler1, C Muchardt, A Suessle
1Department of Medicine, Southwestern Medical School, Dallas, Texas 75235.
Journal of Virology
|February 1, 1994
Summary
The cellular transcription factor PRDII-BF1 activates human immunodeficiency virus (HIV) gene expression by binding to key regulatory elements. This protein enhances HIV-1 LTR activity, independent of the viral tat protein.
Area of Science:
- Molecular Biology
- Virology
- Gene Regulation
Background:
- Human immunodeficiency virus (HIV) gene expression is regulated by cellular transcription factors binding to the HIV-1 long terminal repeat (LTR).
- The NF-kappa B family and other transcription factors, including zinc finger proteins, bind to critical regulatory regions within the HIV-1 LTR.
Purpose of the Study:
- To investigate the role of the zinc finger DNA-binding protein PRDII-BF1 (also known as MBP-1) in modulating HIV-1 gene expression.
- To determine if PRDII-BF1 binds to regulatory elements in the HIV-1 LTR and affects viral gene transcription.
Main Methods:
- DNase I footprinting to identify PRDII-BF1 binding sites on the HIV-1 LTR.
- In vitro translation and vaccinia virus expression to produce full-length PRDII-BF1 protein.
- Transfection experiments using expression vectors and antisense constructs to assess PRDII-BF1's effect on HIV-1 gene expression.
Main Results:
- PRDII-BF1 was shown to bind to both NF-kappa B and TAR (transactivation response) DNA elements within the HIV-1 LTR.
- Expression of full-length PRDII-BF1 protein was confirmed through in vitro and vaccinia virus systems.
- Transfection studies demonstrated that PRDII-BF1 activates HIV-1 gene expression, irrespective of the presence of the viral tat protein.
Conclusions:
- PRDII-BF1 plays a significant role in activating HIV-1 gene expression.
- The findings suggest PRDII-BF1 is a cellular factor that can enhance viral transcription through direct interaction with the HIV-1 LTR.