IκBβ acts to inhibit and activate gene expression during the inflammatory response

Ping Rao, Mathew S. Hayden, Meixiao Long, Martin L. Scott, A. Philip West, Dekai Zhang, Andrea Oeckinghaus, Candace Lynch, Alexander Hoffmann, David Baltimore and Sankar Ghosh ()
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Ping Rao: Yale University School of Medicine
Mathew S. Hayden: Yale University School of Medicine
Meixiao Long: Yale University School of Medicine
Martin L. Scott: California Institute of Technology
A. Philip West: Yale University School of Medicine
Dekai Zhang: Yale University School of Medicine
Andrea Oeckinghaus: Yale University School of Medicine
Candace Lynch: Signaling Systems Laboratory, University of California at San Diego
Alexander Hoffmann: Signaling Systems Laboratory, University of California at San Diego
David Baltimore: California Institute of Technology
Sankar Ghosh: Yale University School of Medicine

Nature, 2010, vol. 466, issue 7310, 1115-1119

Abstract: IκBβ functions revealed The biological role of IκBβ, a major isoform of the IκB (inhibitor of nuclear factor-κB) family of proteins, has proved difficult to establish. Work on mice lacking IκBβ now shows that it serves a dual role, both inhibiting and facilitating the inflammatory response. IκBβ acts through p65:c-Rel dimers to maintain prolonged expression of TNFα. As a result, IκBβ−/− mice are resistant to LPS-induced septic shock and collagen-induced arthritis, and therefore blocking IκBβ might be a promising new strategy for selectively inhibiting the chronic phase of TNFα production during the inflammatory response.

Date: 2010
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DOI: 10.1038/nature09283

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