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

Nicot, Christophe; Mahieux, Renaud; Opavský, René; Cereseto, Anna; Wolff, Linda; Brady, John; Franchini, Genoveffa

doi:10.1038/sj.onc.1203536

Cited by 40 publications

(48 citation statements)

References 72 publications

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“…Earlier studies showed that in the JPX-9 system some Tax-responsive genes displayed signi®cant changes in mRNA levels between 9 and 25 h after metal-induced Tax-expression (Baba et al, 1996;Nagata et al, 1989;Nicot et al, 2000). We thus used for our experiments the 9 and 25 h time points as well as earlier times after metal treatment.…”

Section: Resultsmentioning

confidence: 99%

Genome-wide expression changes induced by HTLV-1 Tax: evidence for MLK-3 mixed lineage kinase involvement in Tax-mediated NF-κB activation

et al. 2001

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The Tax protein of human T-lymphotropic virus type 1 (HTLV-1), an oncoprotein that transactivates viral and cellular genes, plays a key role in HTLV-1 replication and pathogenesis. We used cDNA microarrays to examine Tax-mediated transcriptional changes in the human Jurkat T-cell lines JPX-9 and JPX-M which express Tax and Tax-mutant protein, respectively, under the control of an inducible promoter. Approximately 300 of the over 2000 genes examined were di erentially expressed in the presence of Tax. These genes were grouped according to their function and are discussed in the context of existing ®ndings in the literature. There was strong agreement between our results and genes previously reported as being Tax-responsive. Genes that were di erentially expressed in the presence of Tax included those related to apoptosis, the cell cycle and DNA repair, signaling factors, immune modulators, cytokines and growth factors, and adhesion molecules. Functionally, we provide evidence that one of these genes, the mixed-lineage kinase MLK-3, is involved in Tax-mediated NF-kB signaling. Our current results provide additional insights into Tax-mediated signaling. Oncogene (2001) 20, 4484 ± 4496.

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Section: Resultsmentioning

confidence: 99%

Genome-wide expression changes induced by HTLV-1 Tax: evidence for MLK-3 mixed lineage kinase involvement in Tax-mediated NF-κB activation

et al. 2001

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“…The human T-cell leukemia virus type-1 (HTLV-1), associated with adult T-cell leukemia (ATL), also usurps the NF-kB signaling pathway via its oncoprotein Tax and leads to induction of the antiapoptotic proteins Bcl-xL, Bcl-2 and Bfl-1/A1 to suppress apoptosis and immortalize T cells (Harhaj et al, 1999;Tsukahara et al, 1999;Nicot et al, 2000). Recent studies have shown that Tax undergoes ubiquitination and sumoylation, and that these two modifications act coordinately to regulate Tax localization to nuclear bodies and recruitment of RelA and NEMO to activate NF-kBdependent gene expression (Lamsoul et al, 2005).…”

Section: Update On Nf-jb's Protective Activity Following Viral Infectmentioning

confidence: 99%

Current insights into the regulation of programmed cell death by NF-κB

et al. 2006

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“…Previous studies showed that Tax down-regulates the gene expression of several cellular proteins such as cMyb, DNA polymerase beta, and p18ink4c (Jeang et al, 1990;Lemasson et al, 1997;Nichot et al, 2000;Suzuki et al, 1999). Actually, protein expression levels of c-Myb in HTLV-1-infected cells, which express the Tax protein, are very low (Colgin and Nyborg, 1998;Nichot et al, 2000).…”

mentioning

confidence: 99%

“…Actually, protein expression levels of c-Myb in HTLV-1-infected cells, which express the Tax protein, are very low (Colgin and Nyborg, 1998;Nichot et al, 2000). However, the molecular mechanisms underlying Tax-mediated transcriptional repression remain to be clarified.…”

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confidence: 99%

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The interaction of HTLV-1 Tax with HDAC1 negatively regulates the viral gene expression

2002

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Histone acetyltransferases (HATs) and histone deacetylases (HDACs) are known to interact with several transcription factors and regulate their transcriptional activities. The human T-cell leukemia virus type 1 (HTLV-1) Tax oncoprotein activates transcription from its long terminal repeat (LTR) through interaction with cellular factors such as CREB and a transcriptional coactivator CBP/p300. However, little is known about the interaction between Tax and transcriptional repressors. Here, we demonstrate the physical and functional interaction between Tax and HDAC1. We found that HDAC1 represses the trans-activation function of Tax in 293T and MT4 cells. However, this repression was restored by treatment with an HDAC inhibitor, Trichostatin A. We also observed physical interaction between Tax and HDAC1 both in vitro and in vivo. The N-terminal region of HDAC1 (amino acid residues 28 -97) was required for this binding. Moreover, HDAC1 inhibited the synergistic trans-activation of Tax observed on ectopic expression of CBP. However, this repression was relieved by overexpression of CBP. Thus, HDAC1 is likely to compete with CBP in binding with Tax and functions as a negative regulator for the transcriptional activation by Tax.

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

Cited by 40 publications

References 72 publications

Genome-wide expression changes induced by HTLV-1 Tax: evidence for MLK-3 mixed lineage kinase involvement in Tax-mediated NF-κB activation

Genome-wide expression changes induced by HTLV-1 Tax: evidence for MLK-3 mixed lineage kinase involvement in Tax-mediated NF-κB activation

Current insights into the regulation of programmed cell death by NF-κB

The interaction of HTLV-1 Tax with HDAC1 negatively regulates the viral gene expression

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