Interaction of HTLV-1 Tax1 with p67SRF causes the aberrant induction of cellular immediate early genes through CArG boxes.

Fujii, Masahiro; Tsuchiya, Haruo; Chuhjo, Tatsuya; Akizawa, T; Seiki, Motoharu

doi:10.1101/gad.6.11.2066

Cited by 237 publications

(163 citation statements)

References 51 publications

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“…Similar mechanisms are likely to occur with the transcription factors CREM and ATF-1 Laurance et al, 1997). Tax also induces the activity of the serum responsive elements of various cellular promoters, such as that of the c-fos gene by association with p67 SRF (Fujii et al, 1992). Another important regulatory pathway activated by Tax is that involving the NF-kB/Rel factors.…”

Section: Introductionmentioning

confidence: 92%

The C-terminus of the HTLV-1 Tax oncoprotein mediates interaction with the PDZ domain of cellular proteins

et al. 1998

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Infection by HTLV-1 has been correlated with the appearance of various proliferative or degenerative diseases. Some of these disorders have been observed in transgenic mice expressing the Tax protein, which is known to transactivate various viral and cellular promoters through interactions with several transcription factors. In this study we show that the C-terminus of this viral oncoprotein represents a motif permitting binding of Tax to the PDZ domains of several cellular proteins. A two-hybrid screen with Tax as bait indeed yielded complementary DNAs coding for six proteins including PDZ domains. Two of them correspond to truncated forms of the PSD-95 and b1-syntrophin proteins, another clone codes for a protein homologous to the product of the C. elegans gene lin-7. The other three clones code for new human members of the PDZ family of cellular proteins. The interaction of Tax with the products of these clones was con®rmed by immunoprecipitation assays in mammalian cells, and analysis of various mutants of Tax established the importance of the Cterminal amino acids for several of these interactions. These data suggest that Tax could perturb the normal function of targeted cellular proteins by strongly interacting with their PDZ domains.

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Section: Introductionmentioning

confidence: 92%

The C-terminus of the HTLV-1 Tax oncoprotein mediates interaction with the PDZ domain of cellular proteins

et al. 1998

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“…Tax stimulates transcription through cellular molecules including cAMP-responsive element binding protein (CREB), NF-B and serum responsive factor. [32][33][34] To investigate its potential effect, Tax was transiently transfected together with a human COX-2 promoter reporter construct, phPES2(Ϫ1,439/ϩ59) in Jurkat T cells. Tax increased transcription from the COX-2 promoter by a factor of more than 10-fold (Fig.…”

Section: Role Of Tax In Induction Of the Cox-2 Genementioning

confidence: 99%

Constitutive expression of the cyclooxygenase-2 gene in T-cell lines infected with human T cell leukemia virus type I

Mori

Inoue

Yoshida³

et al. 2001

Int. J. Cancer

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Cyclooxygenase-2 (COX-2), an inducible enzyme that catalyzes the formation of prostaglandins and other eicosanoids from arachidonic acid, is constitutively expressed in several human carcinomas. COX-2 expression, however, has not been extensively studied in leukemia. Human T cell leukemia virus type I (HTLV-I) is the etiologic agent of adult T cell leukemia, an aggressive form of human T cell malignancy. We studied COX-2 mRNA expression in various human Tcell lines. Northern blot analysis revealed that COX-2 mRNA steady-state levels were high in 4 of 7 T-cell lines infected with HTLV-I. COX-2 mRNA, however, was not expressed in any of 3 HTLV-I-negative T-cell lines. We also confirmed COX-2 expression in 6 of 7 HTLV-I-positive T-cell lines by reverse transcription-PCR. HTLV-I Tax is known to increase the expression of cellular genes and thus we assayed Tax for its ability to increase transcription from the COX-2 promoter. Although Tax increased transcription of the COX-2 promoter in a T-cell line, Tax expression did not induce COX-2 mRNA expression, indicating that Tax alone is not sufficient for significant accumulation of COX-2 mRNA, which probably requires an additional viral protein. To evaluate the potential role of COX-2 in T cells, the HTLV-Iinfected T-cell lines were treated with NS398, a selective COX-2 inhibitor. NS398 treatment inhibited proliferation and induced apoptosis of HTLV-I-infected T-cell lines and downregulated Bcl-2 and Bcl-x L mRNA expression, followed by chromosomal DNA fragmentation. Our data suggest that COX-2 is expressed selectively in T-cell lines infected with HTLV-I and that this gene may play a role in cell survival.

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“…pCArG-Luc was constructed by inserting the XbaI-NdeI fragment from pCArG-CAT (Fujii et al, 1992) which contains a CArG box derived from c-fos into the Bg1II-SacI site of PGV-B2 by attaching appropriate linkers at both ends. pIL2R-Luc was constructed by inserting the HindIII-SacI fragment from pRPXbCAT (Maruyama et al, 1987) which has an NF-kB site derived from human IL2Ra chain gene into the HindIII-SacI site of PGV-B2.…”

Section: Plasmid Constructionmentioning

confidence: 99%

Characterization of peripheral blood T-lymphocytes transduced with HTLV-I Tax mutants with different trans-activating phenotypes

Akagi¹,

Ono²,

Nyunoya³

et al. 1997

Oncogene

101

114

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Interaction of HTLV-1 Tax1 with p67SRF causes the aberrant induction of cellular immediate early genes through CArG boxes.

Abstract: Taxl of human T-ceU leukemia virus type 1 (HTLV-1

Cited by 237 publications

References 51 publications

The C-terminus of the HTLV-1 Tax oncoprotein mediates interaction with the PDZ domain of cellular proteins

The C-terminus of the HTLV-1 Tax oncoprotein mediates interaction with the PDZ domain of cellular proteins

Constitutive expression of the cyclooxygenase-2 gene in T-cell lines infected with human T cell leukemia virus type I

Characterization of peripheral blood T-lymphocytes transduced with HTLV-I Tax mutants with different trans-activating phenotypes

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