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Targeting HTLV-1 Activation of NFκB in Mouse Models and ATLL Patients
Viruses 2011, 3(7), 1001-1014; doi:10.3390/v3071001
Review

Anti-Apoptotic Effect of Tax: An NF-κB Path or a CREB Way?

Received: 9 May 2011; in revised form: 9 June 2011 / Accepted: 11 June 2011 / Published: 27 June 2011
(This article belongs to the Special Issue Recent Developments in HTLV Research)
Download PDF [207 KB, uploaded 27 June 2011]
Abstract: The NF-κB pathway is intimately linked to the survival of mammalian cells, and its activation by Tax has consequently been considered important for human T-cell leukemia/lymphoma virus type 1 (HTLV-1)-infected cell resistance to death. Very little emphasis has been given to other mechanisms, although Tax regulates the expression and activity of several cellular genes. The finding that CREB protein is activated in HTLV-1 infected cells underlines the possibility that other mechanisms of survival may be implicated in HTLV-1 infection. Indeed, CREB activation or overexpression plays a role in normal hematopoiesis, as well as in leukemia development, and CREB is considered as a survival factor in various cell systems. A better understanding of the different molecular mechanisms used by Tax to counteract cell death will also help in the development of new therapeutic strategies for HTLV-1 associated diseases.
Keywords: HTLV-1; tax; apoptosis; NF-κB; PI3K/Akt; Ras; ERK; CREB HTLV-1; tax; apoptosis; NF-κB; PI3K/Akt; Ras; ERK; CREB
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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MDPI and ACS Style

Saggioro, D. Anti-Apoptotic Effect of Tax: An NF-κB Path or a CREB Way? Viruses 2011, 3, 1001-1014.

AMA Style

Saggioro D. Anti-Apoptotic Effect of Tax: An NF-κB Path or a CREB Way? Viruses. 2011; 3(7):1001-1014.

Chicago/Turabian Style

Saggioro, Daniela. 2011. "Anti-Apoptotic Effect of Tax: An NF-κB Path or a CREB Way?" Viruses 3, no. 7: 1001-1014.


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