HTLV-1 Tax protein cooperates with Ras in protecting cells from apoptosis

Nicola Vajente, Roberta Trevisan, Daniela Saggioro

Research output: Contribution to journalArticlepeer-review


Tax protein of the human T-cell leukemia virus type 1 (HTLV-1) plays a critical role in HTLV-I-correlated diseases through its ability to deregulate the expression of a vast array of cellular genes. We have previously shown that Tax counteracts apoptosis induced by stimuli triggering mitochondria apoptotic pathway, most likely by activating CREB-mediated transcription and affecting the phosphorylation levels of CREB at Ser-133. Here, we report data that indicate the oncoprotein Ras as a possible mediator of Tax-induced apoptosis protection and suggest a possible role of Tax in Ras activation. In addition, using inhibitors of down stream effectors of Ras, we found that ERK signaling is the most relevant for Tax-mediated apoptosis protection. As a whole, our findings provide intriguing evidence of a possible link between Ras signaling and Tax capability to counteract apoptosis and to enhance P-CREB levels, and implicates a potential role for Ras in HTLV-1-induced diseases.

Original languageEnglish
Pages (from-to)153-163
Number of pages11
Issue number2
Publication statusPublished - Feb 2009


  • Apoptosis
  • Erk1/2
  • GAP
  • HTLV-1
  • Ras
  • Tax

ASJC Scopus subject areas

  • Cancer Research
  • Cell Biology
  • Clinical Biochemistry
  • Biochemistry, medical
  • Pharmaceutical Science
  • Pharmacology


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