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J Biol Chem, Vol. 274, Issue 22, 15297-15300, May 28, 1999
Mediates the Interaction of Cellular I
B Kinases
with the Tax Transforming Protein of Human T Cell Leukemia
Virus Type 1
§,,,§
From the The Tax oncoprotein of human T cell leukemia
virus type 1 constitutively activates transcription factor NF- Howard Hughes Medical Institute and the
§ Department of Microbiology and Immunology, Vanderbilt
University School of Medicine, Nashville, Tennessee 37232-0295 and the
¶ Department of Cancer Biology, Lerner Research Institute,
Cleveland Clinic Foundation, Cleveland, Ohio 44195
B by a
mechanism involving Tax-induced phosphorylation of IB
, a labile
cytoplasmic inhibitor of NF-B. To trigger this signaling cascade,
Tax associates stably with and persistently activates a cellular IB
kinase (IKK) containing both catalytic (IKK and IKK
) and
noncatalytic (IKK
) subunits. We now demonstrate that IKK enables
Tax to dock with the IKK catalytic subunit, resulting in chronic
IB kinase activation. Mutations in either IKK or Tax that prevent
formation of these higher order Tax·IKK complexes also interfere with
the ability of Tax to induce IKK catalytic function in
vivo. Deletion mapping studies indicate that amino acids 1-100
of IKK are required for this Tax targeting function. Together, these
findings identify IKK as an adaptor protein that directs the stable
formation of pathologic Tax·IKK complexes in virally infected T cells.
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