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The NF-kB/Rel transcription factors are present in the cytosol in an inactive state, complexed with the inhibitory IkB proteins. Most agents that activate NF-kB do so through a common pathway based on phosphorylation-induced, proteasome-mediated degradation of IkB. The key regulatory step in this pathway involves activation of a high molecular weight IkB kinase (IKK) complex whose catalysis is generally carried out by three tightly associated IKK subunits. IKK alpha and IKK beta serve as the catalytic subunits of the kinase and IKK gamma serves as the regulatory subunit. Activation of IKK depends upon phosphorylation at Ser177 and Ser181 in the activation loop of IKK beta (Ser176 and Ser180 in IKK alpha), which causes conformational changes, resulting in kinase activation.
I kappa B beta; I(Kappa)B(beta); ikappaBbeta; I-kappa-B-beta; IkB; IKB B; IKB beta; Ikbb; ikB-B; IkBbeta; ikB-beta; NF kappa BIB; NF-kappa-B inhibitor beta; NF-kappa-BIB; NFKB inhibitor beta; NFKBIB; nuclear factor of kappa light chain gene enhancer in B-cells inhibitor, beta; nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, beta; nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, beta; Thyroid receptor; thyroid receptor-interacting protein 9; TR-interacting protein 9; TRIP 9; TRIP9; TRIP-9
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