WIP1 deficiency inhibits HTLV-1 Tax oncogenesis: novel therapeutic prospects for treatment of ATL?

Attenuation of p53 activity appears to be a major step in Human T-lymphotropic virus type 1 (HTLV-1) Tax transformation. However, p53 genomic mutations are late and rather infrequent events in HTLV-1 induced Adult T cell leukemia (ATL). The paper by Zane et al. shows that a mediator of p53 activity,...

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Detalles Bibliográficos
Autores principales: Gillet, Nicolas, Carpentier, Alexandre, Barez, Pierre-Yves, Willems, Luc
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2012
Materias:
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Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3542286/
https://www.ncbi.nlm.nih.gov/pubmed/23256570
http://dx.doi.org/10.1186/1742-4690-9-115
Descripción
Sumario:Attenuation of p53 activity appears to be a major step in Human T-lymphotropic virus type 1 (HTLV-1) Tax transformation. However, p53 genomic mutations are late and rather infrequent events in HTLV-1 induced Adult T cell leukemia (ATL). The paper by Zane et al. shows that a mediator of p53 activity, Wild-type p53-induced phosphatase 1 (Wip1), contributes to Tax-induced oncogenesis in a mouse model. Wip1 may therefore be a novel target for therapeutic approaches.

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