Retroviral oncoprotein Tax induces processing of NF-κB2/p100 in T cells: evidence for the involvement of IKKα

IκB kinase (IKK) is a key mediator of NF‐κB activation induced by various immunological signals. In T cells and most other cell types, the primary target of IKK is a labile inhibitor of NF‐κB, IκBα, which is responsible for the canonical NF‐κB activation. Here, we show that in T cells infected with...

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Bibliographic Details
Published in:The EMBO journal 2001-12, Vol.20 (23), p.6805-6815
Main Authors: Xiao, Gutian, Cvijic, Mary Ellen, Fong, Abraham, Harhaj, Edward W., Uhlik, Mark T., Waterfield, Michael, Sun, Shao-Cong
Format: Article
Language:English
Subjects:
Human T-lymphotropic virus
IKK
IKK^a protein
IKKa protein
NF-^KB protein
NF-κB2 p100-Tax
oncoproteins
p100 protein
p52 protein
proteasome
ubiquitylation
virus-host interaction
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Summary:IκB kinase (IKK) is a key mediator of NF‐κB activation induced by various immunological signals. In T cells and most other cell types, the primary target of IKK is a labile inhibitor of NF‐κB, IκBα, which is responsible for the canonical NF‐κB activation. Here, we show that in T cells infected with the human T‐cell leukemia virus (HTLV), IKKα is targeted to a novel signaling pathway that mediates processing of the nfκb2 precursor protein p100, resulting in active production of the NF‐κB subunit, p52. This pathogenic action is mediated by the HTLV‐encoded oncoprotein Tax, which appears to act by physically recruiting IKKα to p100, triggering phosphorylation‐dependent ubiquitylation and processing of p100. These findings suggest a novel mechanism by which Tax modulates the NF‐κB signaling pathway.
ISSN:0261-4189
1460-2075
DOI:10.1093/emboj/20.23.6805