Author
Listed:
- Ping Rao
(Yale University School of Medicine
Present addresses: Department of Molecular Microbiology and Immunology, University of Southern California, Los Angeles, California 90033, USA (P.R.); Merck Research Laboratories, Boston, Massachusetts 02115, USA (M.L.S.); Center for Extracellular Matrix Biology, Texas A & M University Institute of Biosciences and Technology, Houston, Texas 77030, USA (D.Z.).)
- Mathew S. Hayden
(Yale University School of Medicine
College of Physicians & Surgeons, Columbia University)
- Meixiao Long
(Yale University School of Medicine
College of Physicians & Surgeons, Columbia University)
- Martin L. Scott
(California Institute of Technology
Present addresses: Department of Molecular Microbiology and Immunology, University of Southern California, Los Angeles, California 90033, USA (P.R.); Merck Research Laboratories, Boston, Massachusetts 02115, USA (M.L.S.); Center for Extracellular Matrix Biology, Texas A & M University Institute of Biosciences and Technology, Houston, Texas 77030, USA (D.Z.).)
- A. Philip West
(Yale University School of Medicine)
- Dekai Zhang
(Yale University School of Medicine
Present addresses: Department of Molecular Microbiology and Immunology, University of Southern California, Los Angeles, California 90033, USA (P.R.); Merck Research Laboratories, Boston, Massachusetts 02115, USA (M.L.S.); Center for Extracellular Matrix Biology, Texas A & M University Institute of Biosciences and Technology, Houston, Texas 77030, USA (D.Z.).)
- Andrea Oeckinghaus
(Yale University School of Medicine
College of Physicians & Surgeons, Columbia University)
- 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
College of Physicians & Surgeons, Columbia University)
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.
Suggested Citation
Ping Rao & Mathew S. Hayden & Meixiao Long & Martin L. Scott & A. Philip West & Dekai Zhang & Andrea Oeckinghaus & Candace Lynch & Alexander Hoffmann & David Baltimore & Sankar Ghosh, 2010.
"IκBβ acts to inhibit and activate gene expression during the inflammatory response,"
Nature, Nature, vol. 466(7310), pages 1115-1119, August.
Handle:
RePEc:nat:nature:v:466:y:2010:i:7310:d:10.1038_nature09283
DOI: 10.1038/nature09283
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