scholarly journals Tax protein of human T-cell leukemia virus type I binds to the ankyrin motifs of inhibitory factor kappa B and induces nuclear translocation of transcription factor NF-kappa B proteins for transcriptional activation.

1994 ◽  
Vol 91 (9) ◽  
pp. 3584-3588 ◽  
Author(s):  
H. Hirai ◽  
T. Suzuki ◽  
J. Fujisawa ◽  
J. Inoue ◽  
M. Yoshida
Keyword(s):  
Transcriptional Activation ◽  
Nuclear Translocation ◽  
Leukemia Virus ◽  
Type I ◽  
Cell Leukemia ◽  
Nf Kappa B ◽  
Cell Leukemia Virus Type ◽  
Tax Protein ◽  
Human T Cell ◽  
T Cell Leukemia Virus

scholarly journals Identification of a negative element in the human vimentin promoter: modulation by the human T-cell leukemia virus type I Tax protein.

1993 ◽  
Vol 13 (1) ◽  
pp. 89-97 ◽  
Author(s):  
A Salvetti ◽  
A Lilienbaum ◽  
Z Li ◽  
D Paulin ◽  
L Gazzolo
Keyword(s):  
Binding Site ◽  
Leukemia Virus ◽  
Type I ◽  
Cell Leukemia ◽  
Nf Kappa B ◽  
Cell Leukemia Virus Type ◽  
Negative Region ◽  
Tax Protein ◽  
Human T Cell ◽  
T Cell Leukemia Virus

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)

Identification of a negative element in the human vimentin promoter: modulation by the human T-cell leukemia virus type I Tax protein

1993 ◽  
Vol 13 (1) ◽  
pp. 89-97
Author(s):  
A Salvetti ◽  
A Lilienbaum ◽  
Z Li ◽  
D Paulin ◽  
L Gazzolo
Keyword(s):  
Binding Site ◽  
Leukemia Virus ◽  
Type I ◽  
Cell Leukemia ◽  
Nf Kappa B ◽  
Cell Leukemia Virus Type ◽  
Negative Region ◽  
Tax Protein ◽  
Human T Cell ◽  
T Cell Leukemia Virus

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)

Kinetic analysis of human T-cell leukemia virus type I Tax-mediated activation of NF-kappa B

1994 ◽  
Vol 14 (10) ◽  
pp. 6443-6451
Author(s):  
T Kanno ◽  
K Brown ◽  
G Franzoso ◽  
U Siebenlist
Keyword(s):  
T Cell ◽  
Leukemia Virus ◽  
Type I ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
Nf Kappa B ◽  
Cell Leukemia Virus Type ◽  
I Kappa B Alpha ◽  
Human T Cell ◽  
T Cell Leukemia Virus

The human T-cell leukemia virus type I (HTLV-I) Tax protein induces the expression of cellular genes, at least in part, by activating the endogenous NF-kappa B transcription factors. Induced expression of cellular genes is thought to be important for transformation of T cells to continued growth, a prelude to the establishment of adult T-cell leukemia. However, neither underlying mechanisms nor kinetics of the Tax-mediated activation of NF-kappa B are understood. We have analyzed a permanently transfected Jurkat T-cell line in which the expression of Tax is entirely dependent on addition of heavy metals. The initial NF-kappa B binding activity seen after induction of Tax is due almost exclusively to p50/p65 heterodimers. At later times, NF-kappa B complexes containing c-Rel and/or p52 accumulate. The early activation of p50/p65 complexes is a posttranslational event, since neither mRNA nor protein levels of NF-kappa B subunits had increased at that time. We demonstrate for the first time a Tax-induced proteolytic degradation of the NF-kappa B inhibitor, I kappa B-alpha, which may trigger the initial nuclear translocation of NF-kappa B. As nuclear NF-kappa B rapidly and potently stimulates resynthesis of I kappa B-alpha, the steady-state level of I kappa B-alpha does not significantly change. Thus, the dramatic Tax-induced increase in the I kappa B-alpha turnover may continually weaken inhibition and activate NF-kappa B. Additional, distinct actions of Tax may contribute further to the high levels of NF-kappa B activity seen.

scholarly journals Kinetic analysis of human T-cell leukemia virus type I Tax-mediated activation of NF-kappa B.

1994 ◽  
Vol 14 (10) ◽  
pp. 6443-6451 ◽  
Author(s):  
T Kanno ◽  
K Brown ◽  
G Franzoso ◽  
U Siebenlist
Keyword(s):  
T Cell ◽  
Leukemia Virus ◽  
Type I ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
Nf Kappa B ◽  
Cell Leukemia Virus Type ◽  
I Kappa B Alpha ◽  
Human T Cell ◽  
T Cell Leukemia Virus

The human T-cell leukemia virus type I (HTLV-I) Tax protein induces the expression of cellular genes, at least in part, by activating the endogenous NF-kappa B transcription factors. Induced expression of cellular genes is thought to be important for transformation of T cells to continued growth, a prelude to the establishment of adult T-cell leukemia. However, neither underlying mechanisms nor kinetics of the Tax-mediated activation of NF-kappa B are understood. We have analyzed a permanently transfected Jurkat T-cell line in which the expression of Tax is entirely dependent on addition of heavy metals. The initial NF-kappa B binding activity seen after induction of Tax is due almost exclusively to p50/p65 heterodimers. At later times, NF-kappa B complexes containing c-Rel and/or p52 accumulate. The early activation of p50/p65 complexes is a posttranslational event, since neither mRNA nor protein levels of NF-kappa B subunits had increased at that time. We demonstrate for the first time a Tax-induced proteolytic degradation of the NF-kappa B inhibitor, I kappa B-alpha, which may trigger the initial nuclear translocation of NF-kappa B. As nuclear NF-kappa B rapidly and potently stimulates resynthesis of I kappa B-alpha, the steady-state level of I kappa B-alpha does not significantly change. Thus, the dramatic Tax-induced increase in the I kappa B-alpha turnover may continually weaken inhibition and activate NF-kappa B. Additional, distinct actions of Tax may contribute further to the high levels of NF-kappa B activity seen.

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