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.