Dialyzable Leukocyte Extract Suppresses the Activity of Essential Transcription Factors for HIV-1 Gene Expression in Unstimulated MT-4 Cells

2000 ◽  
Vol 273 (3) ◽  
pp. 1099-1103 ◽  
Author(s):  
Miriam Ojeda Ojeda ◽  
Celia Fernández-Ortega ◽  
Manuel de J.Arana Rosaínz
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Hiv 1

Regulation of HIV-1 Gene Expression by Cellular Transcription Factors

Pathobiology ◽  
1992 ◽  
Vol 60 (4) ◽  
pp. 219-224 ◽  
Author(s):  
Premkumar Ready ◽  
Purandar Dasgupta
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Cellular Transcription ◽  
Hiv 1

scholarly journals Nucleosomes and regulation of gene expression. Structure of the HIV-1 5'LTR.

1998 ◽  
Vol 45 (1) ◽  
pp. 209-219 ◽  
Author(s):  
P Widłak ◽  
W T Garrard
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Chromatin Remodeling ◽  
Binding Sites ◽  
Regulation Of Gene Expression ◽  
Dnase I ◽  
Chromatin Assembly ◽  
Hypersensitive Sites ◽  
Hiv 1

Packaging of DNA into chromatin adds complexity to the problem of regulation of gene expression. Nucleosomes affect the accessibility of transcription factors to occupy their binding sites in chromatin of eukaryotic cells. The disruption of nucleosome structure within the enhancer/promoter region of the integrated HIV-1 proviral genome is an instructive example of a chromatin remodeling process during transcriptional activation. To investigate the mechanism responsible for generating nuclease hypersensitive sites that exist in vivo in the promoter/enhancer region of the 5'LTR (long terminal repeat) of integrated HIV-1 we have utilized an in vitro chromatin assembly system with Xenopus oocyte extracts. Chromatin assembly in the presence of Sp1 and NFkappaB transcription factors induces DNase I hypersensitive sites on either side of their binding sites and positions the adjacent nucleosomes. This structure can also be formed in a factor-induced, ATP-dependent chromatin remodeling process and closely resembles the in vivo chromatin structure. The DNase I hypersensitive sites that form within the HIV LTR are probably histone-free and remain after removal of transcription factors.

scholarly journals T Cell Activation and Regulation of HIV-1: Same Effectors with Distinct Outcomes

1999 ◽  
Vol 10 (suppl c) ◽  
pp. 25C-32C ◽  
Author(s):  
Jean-François Fortin ◽  
Benoit Barbeau ◽  
Gilles A Robichaud ◽  
Michel J Tremblay
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Immune System ◽  
Virus Replication ◽  
T Cell Activation ◽  
Cell Activation ◽  
Molecular Mechanisms ◽  
Nuclear Factor ◽  
Cellular Transcription ◽  
Hiv 1

The molecular mechanisms that regulate the function of the immune system and human immunodeficiency virus type-1 (HIV-1) gene expression are diverse and complicated. However, replication of HIV-1 is controlled by many of the same regulatory signals that play a crucial role in the transcriptional regulation of the immune system. For example, the viral promoter, as is the case for the immune system, is subject to complex regulation by combinations of cellular transcription factors that may quantitatively and/or qualitatively differ depending on cell types (eg, macrophages versus T lymphocytes) and cell states (eg, undifferentiated versus differentiated or quiescent versus activated). The present review discusses the regulation of HIV-1 gene expression by nuclear factor-kappa Band nuclear factor of activated T cells, and proposes that selective interference of these two cellular transcription factors may be a route to abrogate virus replication without disrupting normal cellular functions. A better understanding of the regulation of HIV-1 gene expression is of utmost importance for the design of molecular approaches that will effectively abrogate virus replication and, ultimately, disease progression.

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