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. 2018 Nov 28;9:2620. doi: 10.3389/fimmu.2018.02620

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Copyright © 2018 Beling and Kespohl.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Regulation of NF-κB signaling by the proteasome. Multiple inflammatory signals result in the activation of the transcription factor NF-κB through a variety of adapter proteins and kinases. The most abundant form of the NF-κB dimer is the p50/p65 heterodimer. (A) The p105 precursor is processed by the proteasome, thereby liberating the NF-kB p50 subunit for dimerization with p65. IκB retains the NF-κB heterodimer in the cytoplasm. (B) Ligand binding to cellular receptors like TLRs activates the IKK complex, which catalyzes the phosphorylation of IκB, inducing its poly-ubiquitination and degradation by the proteasome. (C) Activated NF-κB translocates into the nucleus, where it (D) activates target gene expression. Table 2 summarizes all reported effects of i-proteasome activity on the different steps in this canonical NF-κB signaling pathway. NF-kB, nuclear factor kappa B; IκBs, inhibitors of κB; IKK, IκB kinase.