Anti-Apoptotic Effect of Tax: An NF-κB Path or a CREB Way?
2011
Anti-Apoptotic Effect of Tax: An NF-κB Path or a CREB Way?
publication
Evidence: moderate
Author Information
Author(s): Saggioro Daniela
Primary Institution: Veneto Institute of Oncology IOV-IRCCS
Hypothesis
The study investigates the mechanisms by which the Tax protein of HTLV-1 prevents apoptosis in infected cells.
Conclusion
The Tax protein activates multiple survival pathways, including NF-κB and CREB, to inhibit apoptosis in HTLV-1-infected cells.
Supporting Evidence
- The Tax protein is considered the main oncogenic product of HTLV-1.
- Tax activates the NF-κB pathway, which is crucial for the survival of HTLV-1-infected cells.
- CREB activation is also implicated in the anti-apoptotic effects of Tax.
Takeaway
The Tax protein from a virus helps infected cells live longer by turning on special signals that stop them from dying.
Methodology
The review discusses various signaling pathways activated by the Tax protein, including NF-κB, PI3K/Akt, and CREB.
Limitations
The review primarily focuses on the mechanisms of Tax without experimental data to support the claims.
Digital Object Identifier (DOI)
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