An Exposed KID-Like Domain in Human T-Cell Lymphotropic Virus Type 1 Tax Is Responsible for the Recruitment of Coactivators CBP/p300

Harrod, Robert; Tang, Yong; Nicot, Christophe; Lu, Hsieng S.; Vassilev, Alex; Nakatani, Yoshihiro; Giam, Chou-Zen

doi:10.1128/mcb.18.9.5052

Cited by 170 publications

(252 citation statements)

References 56 publications

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“…As shown in Figure 2, most of the previously reported Tax domains were conserved in human and simian Tax3 sequences. Of interest, the Tax3 putative KID-like-binding domain sequence (aa 81-95) (Harrod et al, 1998) is very similar to that of Tax1 and of Tax2, with one amino-acid change as compared to Tax2a and two as compared to Tax1 and Tax2b. Interestingly, the two amino acids corresponding to the M22 domain (aa 130-131) (Smith and Greene, 1990) are modified in the Tax3 vs Tax1 protein.…”

Section: Resultsmentioning

confidence: 99%

“…Given that binding to the co-activators is critical for Tax1 and Tax2-mediated transactivation (Kwok et al, 1996;Harrod et al, 1998;Kashanchi et al, 1998;Meertens et al, 2004b), we also undertook a series of experiments aiming at determining whether Tax3 could bind the CBP and p300 coactivators. Using the GFP, GFP-Tax1, GFP-Tax2 and GFP-Tax3 S proteins Characterization of the HTLV/STLV-3 Tax protein SA Chevalier et al expressed from 293T-transfected cells, we performed a series of co-immunoprecipitations as previously described (Meertens et al, 2004b).…”

Section: Resultsmentioning

confidence: 99%

“…To compare the interactions of Tax1 and Tax3 S with p300 and CBP, we performed another series of experiments using purified Tax1 and Tax3 together with several GST-CBP and GST-p300 constructs that contain either the CH/1, and/or the KIX or the C/H2 domains. Both C/H1 and KIX domains have been shown to bind Tax1 (Harrod et al, 1998;Lemasson and Nyborg, 2001). Interestingly, Tax3 To determine whether Tax3 is a viral transactivator, we then investigated whether the purified Tax3 protein was able to activate transcription from an HTLVderived promoter.…”

Section: Resultsmentioning

confidence: 99%

“…Of note, we have observed that, while the interaction of Tax1 and Tax3 with CBP was equivalent, Tax3 binding to p300 seemed weaker than that of Tax1. Tax1 has been shown to bind at least three separate domains of CBP, which include the KIX domain, the C/H1 domain and the CR2 domain (Harrod et al, 1998;Lemasson and Nyborg, 2001;Scoggin et al, 2001). To our knowledge, with the exception of the CR2 domain, these important experiments have only been conducted with CBP protein fragments.…”

Section: Characterization Of the Htlv/stlv-3 Tax Proteinmentioning

confidence: 99%

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The tax protein from the primate T-cell lymphotropic virus type 3 is expressed in vivo and is functionally related to HTLV-1 Tax rather than HTLV-2 Tax

et al. 2006

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Human T-cell leukemia virus and simian T-cell leukemia virus (STLV) form the primate T-cell lymphotropic viruses group. Human T-cell leukemia virus type 1 and type 2 (HTLV-1 and HTLV-2) encode the Tax viral transactivator (Tax1 and Tax2, respectively). Tax1 possesses an oncogenic potential and is responsible for cell transformation both in vivo and in vitro. We and others have recently discovered the existence of human Tcell lymphotropic virus type 3. However, there is currently no evidence for the presence of a Tax protein in HTLV-3-infected individuals. We show that the serum of an HTLV-3 asymptomatic carrier and the sera of two STLV-3-infected monkeys contain specific anti-Tax3 antibodies. We also show that tax3 mRNA is present in the PBMCs obtained from an STLV-3-infected monkey, demonstrating that Tax3 is expressed in vivo. We further demonstrate that Tax3 intracellular localization is very similar to that of Tax1 and that Tax3 binds to both CBP and p300 coactivators. Using purified Tax3, we show that the protein increases transcription from a 4TxRE G-free cassette plasmid in an in vitro transcription assay. In all cell types tested, including transiently transfected lymphocytes, Tax3 activates its own promoter STLV-3 long terminal repeat (LTR), which contains only two Tax Responsive Elements (TREs), and activates also HTLV-1 and HTLV-2 LTRs. In addition, Tax3 also activates the NF-jB pathway. We also show that Tax3 possesses a PDZ-binding sequence at its C-terminal end. Our results demonstrate that Tax3 is a transactivator, and that its properties are more similar to that of Tax1, rather than of Tax2. This suggests the possible occurrence of lymphoproliferative disorders among HTLV-3-infected populations.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Characterization Of the Htlv/stlv-3 Tax Proteinmentioning

confidence: 99%

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The tax protein from the primate T-cell lymphotropic virus type 3 is expressed in vivo and is functionally related to HTLV-1 Tax rather than HTLV-2 Tax

et al. 2006

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“…The pleiotropic e ects of Tax result from its ability to activate transcription through distinct pathways, including CREB/ATF, NF-kB and SRE, and to alter the expression of numerous cellular genes. Tax can engage itself in a multi-protein complex, including CREB and CBP/p300, essential for Tax stimulation of transcription from the viral LTR (Giebler et al, 1997;Harrod et al, 1998). In addition, Tax has been shown to repress cellular promoters containing E-box motifs such as the b-polymerase and Lck (Jeang et al, 1990;Lemasson et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

HTLV-I Tax transrepresses the human c-Myb promoter independently of its interaction with CBP or p300

et al. 2000

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Impact of transforming viruses on cellular mutagenesis, genome stability, and cellular transformation

Gatza

Chandhasin

Ducu

et al. 2005

Environ and Mol Mutagen

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It is estimated that 15% of all cancers are etiologically linked to viral infection. Specific cancers including adult T-cell leukemia, hepatocellular carcinoma, and uterine cervical cancer are associated with infection by human T-cell leukemia virus type I, hepatitis B virus, and high-risk human papilloma virus, respectively. In these cancers, genomic instability, a hallmark of multistep cancers, has been explicitly linked to the expression of oncoproteins encoded by these viruses. This review discusses mechanisms utilized by these viral oncoproteins, Tax, HBx, and E6/E7, to mediate genomic instability and cellular transformation.

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An Exposed KID-Like Domain in Human T-Cell Lymphotropic Virus Type 1 Tax Is Responsible for the Recruitment of Coactivators CBP/p300

Cited by 170 publications

References 56 publications

The tax protein from the primate T-cell lymphotropic virus type 3 is expressed in vivo and is functionally related to HTLV-1 Tax rather than HTLV-2 Tax

The tax protein from the primate T-cell lymphotropic virus type 3 is expressed in vivo and is functionally related to HTLV-1 Tax rather than HTLV-2 Tax

HTLV-I Tax transrepresses the human c-Myb promoter independently of its interaction with CBP or p300

Impact of transforming viruses on cellular mutagenesis, genome stability, and cellular transformation

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