Tax-induced HTLV-I LTR transcriptional activation is modulated by phosphorylation

D. Saggioro, M. Forino, A. Penzo, M. Pesce, S. Oliviero, L. Chieco-Bianchi

Research output: Contribution to journalArticlepeer-review


We studied the effect of protein phosphatase and kinase inhibitors on Tax-mediated transcription of constructs carrying the receptor gene chloramphenicol acetyl transferase under the control of either the full-length LTR of HTLV-I or three copies of the tax-responsive 21-bp repeats. We observed that treatment with okadaic acid, which inhibits the serine/threonine protein phosphatases type 1 and 2A, reduced HTLV-I LTR, transcriptional activation in MT2 and K562 cells; on the contrary, the enhancer activity of the 21-bp sequences was significantly increased in both cell lines; treatment with the protein kinase C inhibitor H-7 blocked Tax-mediated transcription of both constructs. We also found that treatment with sodium orthovanadate, a tyrosine phosphatase inhibitor, reduced Tax-mediated activation of both plasmids. These findings indicated that specific serine/threonine phosphorylation events are required for Tax-mediated HTLV-1 LTR activation and also suggested that phosphorylation at tyrosine residues is involved in this process.

Original languageEnglish
Pages (from-to)666-673
Number of pages8
JournalBiochemical and Biophysical Research Communications
Issue number1
Publication statusPublished - 1994

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology


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