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Retroviral oncoprotein Tax induces processing of NF‐κB2/p100 in T cells: evidence for the involvement of IKKα
Author(s) -
Xiao Gutian,
Cvijic Mary Ellen,
Fong Abraham,
Harhaj Edward W.,
Uhlik Mark T.,
Waterfield Michael,
Sun ShaoCong
Publication year - 2001
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/20.23.6805
Subject(s) - biology , iκb kinase , signal transduction , phosphorylation , nf κb , microbiology and biotechnology , ubiquitin , nfkb1 , cancer research , biochemistry , gene , transcription factor
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.