Journal
APOPTOSIS
Volume 14, Issue 2, Pages 153-163Publisher
SPRINGER
DOI: 10.1007/s10495-008-0289-3
Keywords
Tax; Ras; Erk1/2; HTLV-1; GAP(1m); Apoptosis
Categories
Funding
- European Union [2005-018704]
- Associazione Italiana per la Ricerca sul Cancro
- Ministero della Salute [RFPS-2006-2342010]
- Fondazione Italiana per la Ricerca sul Cancro
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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.
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