IκBβ enhances the generation of the low-affinity NFκB/RelA homodimer

Rachel Tsui, Jeffrey D. Kearns, Candace Lynch, Don Vu, Kim A. Ngo, Soumen Basak, Gourisankar Ghosh and Alexander Hoffmann ()
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Rachel Tsui: Signaling Systems Laboratory, University of California
Jeffrey D. Kearns: Signaling Systems Laboratory, University of California
Candace Lynch: Signaling Systems Laboratory, University of California
Don Vu: University of California
Kim A. Ngo: Signaling Systems Laboratory, University of California
Soumen Basak: Signaling Systems Laboratory, University of California
Gourisankar Ghosh: University of California
Alexander Hoffmann: Signaling Systems Laboratory, University of California

Nature Communications, 2015, vol. 6, issue 1, 1-10

Abstract: Abstract The NFκB family of dimeric transcription factors regulate inflammatory and immune responses. While the dynamic control of NFκB dimer activity via the IκB–NFκB signalling module is well understood, there is little information on how specific dimer repertoires are generated from Rel family polypeptides. Here we report the iterative construction—guided by in vitro and in vivo experimentation—of a mathematical model of the Rel-NFκB generation module. Our study reveals that IκBβ has essential functions within the Rel-NFκB generation module, specifically for the RelA:RelA homodimer, which controls a subset of NFκB target genes. Our findings revise the current dogma of the three classical, functionally related IκB proteins by distinguishing between a positive ‘licensing’ factor (IκBβ) that contributes to determining the available NFκB dimer repertoire in a cell’s steady state, and negative feedback regulators (IκBα and -ɛ) that determine the duration and dynamics of the cellular response to an inflammatory stimulus.

Date: 2015
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DOI: 10.1038/ncomms8068

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