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Persistent activation of NF-kappaB by the tax transforming protein of HTLV-1: hijacking cellular IkappaB kinases Sun SC; Ballard DWOncogene 1999[Nov]; 18 (49): 6948-58Biochemical coupling of transcription factor NF-kappaB to antigen and co-stimulatory receptors is required for the temporal control of T-cell proliferation. In contrast to its transitory activation during normal growth-signal transduction, NF-kappaB is constitutively deployed in T-cells transformed by the type 1 human T-cell leukemia virus (HTLV-1). This viral/host interaction is mediated by the HTLV-1-encoded Tax protein, which has potent oncogenic properties. As reviewed here, Tax activates NF-kappaB primarily via a pathway leading to the chronic phosphorylation and degradation of IkappaBalpha, a cytoplasmic inhibitor of NF-kappaB. To access this pathway, Tax associates stably with a cytokine-inducible IkappaB kinase (IKK), which contains both catalytic (IKKalpha and IKKbeta) and noncatalytic (IKKgamma) subunits. Unlike their transiently induced counterparts in cytokine-treated cells, Tax-associated forms of IKKalpha and IKKbeta are persistently activated in HTLV-1-infected T cells. Acquisition of the deregulated IKK phenotype is contingent on the presence of IKKgamma, which functions as a molecular adaptor in the assembly of pathologic Tax/IkappaB kinase complexes. These findings highlight a key mechanistic role for IKK in the Tax/NF-kappaB signaling axis and define new intracellular targets for the therapeutic control of HTLV-1-associated disease.|Animals[MESH]|Cysteine Endopeptidases/physiology[MESH]|Gene Products, tax/*physiology[MESH]|Human T-lymphotropic virus 1/*physiology[MESH]|Humans[MESH]|I-kappa B Kinase[MESH]|Multienzyme Complexes/physiology[MESH]|NF-kappa B/*physiology[MESH]|Proteasome Endopeptidase Complex[MESH]|Protein Serine-Threonine Kinases/*physiology[MESH]|Signal Transduction[MESH] |
