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EMBO J ; 20(23): 6805-15, 2001 Dec 03.
Article in English | MEDLINE | ID: mdl-11726516

ABSTRACT

IkappaB kinase (IKK) is a key mediator of NF-kappaB 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-kappaB, IkappaBalpha, which is responsible for the canonical NF-kappaB activation. Here, we show that in T cells infected with the human T-cell leukemia virus (HTLV), IKKalpha is targeted to a novel signaling pathway that mediates processing of the nfkappab2 precursor protein p100, resulting in active production of the NF-kappaB subunit, p52. This pathogenic action is mediated by the HTLV-encoded oncoprotein Tax, which appears to act by physically recruiting IKKalpha to p100, triggering phosphorylation-dependent ubiquitylation and processing of p100. These findings suggest a novel mechanism by which Tax modulates the NF-kappaB signaling pathway.


Subject(s)
Gene Products, tax/metabolism , NF-kappa B/metabolism , Protein Serine-Threonine Kinases/metabolism , T-Lymphocytes/metabolism , Amino Acid Sequence , Cell Line , Enzyme Activation , Genes, Dominant , Genes, Reporter , Green Fluorescent Proteins , Human T-lymphotropic virus 1/metabolism , Humans , I-kappa B Kinase , Immunoblotting , Jurkat Cells , Luciferases/metabolism , Luminescent Proteins/metabolism , Molecular Sequence Data , NF-kappa B p52 Subunit , Phosphorylation , Plasmids/metabolism , Protein Binding , Protein Structure, Tertiary , Retroviridae/genetics , Retroviridae/metabolism , Signal Transduction , Time Factors , Transfection , Ubiquitin/metabolism , Viral Envelope Proteins/metabolism
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