Activation of IKKα and IKKβ through their fusion with HTLV-I Tax protein

摘要: Human T-cell leukemia virus type I (HTLV-I) Tax protein persistently stimulates the activity of IκB kinase (IKK), resulting in constitutive activation transcription factor NF-κB. IKK requires physical interaction this viral with regulatory subunit, IKKγ. The Tax/IKKγ allows to engage catalytic subunits, IKKα and IKKβ, although it remains unclear whether linker function IKKγ is sufficient for supporting Tax-specific activation. To address question, we have examined sequences required modulating Tax/IKK signaling. We demonstrate that when fused Tax, a small N-terminal fragment IKKγ, containing its minimal IKKα/β-binding domain, bringing activating subunits. Disruption domain abolishes further direct fusion IKKβ leads these kinases. These findings suggest IKKγ-directed association serves as molecular trigger