IKKγ Mediates the Interaction of Cellular IκB Kinases with the Tax Transforming Protein of Human T Cell Leukemia Virus Type 1
作者： Zhi-Liang Chu , Young-Ah Shin , Jin-Ming Yang , Joseph A. DiDonato , Dean W. Ballard
关键词: Virology 、 Cell biology 、 IκB kinase 、 Transcription factor 、 Phosphorylation 、 Cytoplasm 、 Signal transducing adaptor protein 、 Kinase 、 IκBα 、 Protein subunit 、 Biology
摘要: The Tax oncoprotein of human T cell leukemia virus type 1 constitutively activates transcription factor NF-κB by a mechanism involving Tax-induced phosphorylation IκBα, labile cytoplasmic inhibitor NF-κB. To trigger this signaling cascade, associates stably with and persistently cellular IκB kinase (IKK) containing both catalytic (IKKα IKKβ) noncatalytic (IKKγ) subunits. We now demonstrate that IKKγ enables to dock the IKKβ subunit, resulting in chronic activation. Mutations either or prevent formation these higher order Tax·IKK complexes also interfere ability induce function vivo. Deletion mapping studies indicate amino acids 1–100 are required for targeting function. Together, findings identify as an adaptor protein directs stable pathologic virally infected cells.
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