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Journal of Cancer Research and Clinical Oncology logoLink to Journal of Cancer Research and Clinical Oncology
. 1995 Sep;121(9-10):521–528. doi: 10.1007/BF01197764

HTLV-1 oncoprotein Tax deregulates transcription of cellular genes through multiple mechanisms

Mitsuaki Yoshida 1
PMCID: PMC12201570  PMID: 7559731

Abstract

Infection of a human retrovirus HTLV-1 induces adult T cell leukemia and a neurological disease, HAM/TSP. Regulatory protein Tax of HTLV-1 is thought to contribute to the pathogenesis. We have studied the mechanism of transcriptional activation induced by Tax protein and identified two independent mechanisms: (a) binding to the enhancer-binding proteins, CREB, CREM, NF-κB and SRF, resulting in the activation of these factors through indirect binding to each specific DNA sequence, and (b) binding to IκB protein resulting in the suppression of the negative regulator IκB, which binds to NF-κB. In addition to these factors, a new protein GLI/THP is also involved in the transactivation. On the basis of these mechanisms, gene regulations in vitro and in vivo in HTLV-1-infected cells are discussed.

Key words: HTLV-1; Transcriptional activation; ATL; NF-κB, IκB

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