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

G. Xiao, M. E. Cvijic, A. Fong, E. W. Harhaj, M. T. Uhlik, M. Waterfield, S. C. Sun

Research output: Contribution to journalArticlepeer-review

245 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)6805-6815
Number of pages11
JournalEMBO Journal
Volume20
Issue number23
DOIs
StatePublished - Dec 3 2001

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Molecular Biology
  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Microbiology(all)

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