scholarly journals Identification of an NF-kappa B binding site in the bovine leukemia virus promoter.

1995 ◽  
Vol 69 (10) ◽  
pp. 6005-6009 ◽  
Author(s):  
P A Brooks ◽  
J K Nyborg ◽  
G L Cockerell
2010 ◽  
Vol 285 (25) ◽  
pp. 19434-19449 ◽  
Author(s):  
Valérie Pierard ◽  
Allan Guiguen ◽  
Laurence Colin ◽  
Gaëlle Wijmeersch ◽  
Caroline Vanhulle ◽  
...  

1998 ◽  
Vol 72 (7) ◽  
pp. 5526-5534 ◽  
Author(s):  
Véronique Kiermer ◽  
Carine Van Lint ◽  
Delphine Briclet ◽  
Caroline Vanhulle ◽  
Richard Kettmann ◽  
...  

ABSTRACT Bovine leukemia virus (BLV) replication is controlled by bothcis- and trans-acting elements. The virus-encoded transactivator, Tax, is necessary for efficient transcription from the BLV promoter, although it is not present during the early stages of infection. Therefore, sequences that control Tax-independent transcription must play an important role in the initiation of viral gene expression. This study demonstrates that the R-U5 sequence of BLV stimulates Tax-independent reporter gene expression directed by the BLV promoter. R-U5 was also stimulatory when inserted immediately downstream from the transcription initiation site of a heterologous promoter. Progressive deletion analysis of this region revealed that a 46-bp element corresponding to the 5′ half of U5 is principally responsible for the stimulation. This element exhibited enhancer activity when inserted upstream or downstream from the herpes simplex virus thymidine kinase promoter. This enhancer contains a binding site for the interferon regulatory factors IRF-1 and IRF-2. A 3-bp mutation that destroys the IRF recognition site caused a twofold decrease in Tax-independent BLV long terminal repeat-driven gene expression. These observations suggest that the IRF binding site in the U5 region of BLV plays a role in the initiation of virus replication.


2007 ◽  
Vol 282 (29) ◽  
pp. 20854-20867 ◽  
Author(s):  
Thi Lien-Anh Nguyên ◽  
Stéphane de Walque ◽  
Emmanuelle Veithen ◽  
Ann Dekoninck ◽  
Valérie Martinelli ◽  
...  

1993 ◽  
Vol 13 (1) ◽  
pp. 89-97 ◽  
Author(s):  
A Salvetti ◽  
A Lilienbaum ◽  
Z Li ◽  
D Paulin ◽  
L Gazzolo

The vimentin gene is a member of the intermediate filament multigene family and encodes a protein expressed, in vivo, in all mesenchymal derivatives and, in vitro, in cell types of various origin. We have previously demonstrated that the expression of this growth-regulated gene could be trans activated by the 40-kDa Tax protein of HTLV-I (human T-cell leukemia virus type I) and that responsiveness to this viral protein was mediated by the presence of an NF-kappa B binding site located between -241 and -210 bp upstream of the mRNA cap site (A. Lilienbaum, M. Duc Dodon, C. Alexandre, L. Gazzolo, and D. Paulin, J. Virol. 64:256-263, 1990). These previous assays, performed with deletion mutants of the vimentin promoter linked to the chloramphenicol acetyltransferase gene, also revealed the presence of an upstream negative region between -529 and -241 bp. Interestingly, the inhibitory activity exerted by this negative region was overcome after cotransfection of a Tax-expressing plasmid. In this study, we further characterize the vimentin negative element and define the effect of the Tax protein on the inhibitory activity of this element. We first demonstrate that a 187-bp domain (-424 to -237 bp) behaves as a negative region when placed upstream either of the NF-kappa B binding site of vimentin or of a heterologous enhancer such as that present in the desmin gene promoter. The negative effect can be further assigned to a 32-bp element which is indeed shown to repress the basal or induced activity of the NF-kappa B binding site.(ABSTRACT TRUNCATED AT 250 WORDS)


1993 ◽  
Vol 13 (1) ◽  
pp. 89-97
Author(s):  
A Salvetti ◽  
A Lilienbaum ◽  
Z Li ◽  
D Paulin ◽  
L Gazzolo

The vimentin gene is a member of the intermediate filament multigene family and encodes a protein expressed, in vivo, in all mesenchymal derivatives and, in vitro, in cell types of various origin. We have previously demonstrated that the expression of this growth-regulated gene could be trans activated by the 40-kDa Tax protein of HTLV-I (human T-cell leukemia virus type I) and that responsiveness to this viral protein was mediated by the presence of an NF-kappa B binding site located between -241 and -210 bp upstream of the mRNA cap site (A. Lilienbaum, M. Duc Dodon, C. Alexandre, L. Gazzolo, and D. Paulin, J. Virol. 64:256-263, 1990). These previous assays, performed with deletion mutants of the vimentin promoter linked to the chloramphenicol acetyltransferase gene, also revealed the presence of an upstream negative region between -529 and -241 bp. Interestingly, the inhibitory activity exerted by this negative region was overcome after cotransfection of a Tax-expressing plasmid. In this study, we further characterize the vimentin negative element and define the effect of the Tax protein on the inhibitory activity of this element. We first demonstrate that a 187-bp domain (-424 to -237 bp) behaves as a negative region when placed upstream either of the NF-kappa B binding site of vimentin or of a heterologous enhancer such as that present in the desmin gene promoter. The negative effect can be further assigned to a 32-bp element which is indeed shown to repress the basal or induced activity of the NF-kappa B binding site.(ABSTRACT TRUNCATED AT 250 WORDS)


Oncogene ◽  
2003 ◽  
Vol 22 (19) ◽  
pp. 2882-2896 ◽  
Author(s):  
Ann Dekoninck ◽  
Claire Calomme ◽  
Séverine Nizet ◽  
Yvan de Launoit ◽  
Arsène Burny ◽  
...  

Author(s):  
N.V. Bateneva ◽  
◽  
P.N. Smirnov ◽  
I.V. Mikhnovich ◽  
◽  
...  

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