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- Title
Association of β-arrestin and TRAF6 negatively regulates Toll-like receptor–interleukin 1 receptor signaling.
- Authors
Yaya Wang; Yawei Tang; Lin Teng; Yalan Wu; Xiaohui Zhao; Gang Pei
- Abstract
Tumor necrosis factor receptor–associated factor 6 (TRAF6) is critical for mediating Toll-like receptor (TLR)–interleukin 1 receptor (IL-1R) signaling and subsequent activation of NF-κB and AP-1, transcriptional activators of innate immunity. Here we show that β-arrestins, a family of multifunctional proteins, directly interacted with TRAF6 after TLR–IL-1R activation. Formation of the β-arrestin–TRAF6 complex prevented autoubiquitination of TRAF6 and activation of NF-κB and AP-1. Endotoxin-treated β-arrestin 2–deficient mice had higher expression of proinflammatory cytokines and were more susceptible to endotoxic shock. Thus, β-arrestins are essential negative regulators of innate immune activation via TLR–IL-1R signaling.
- Publication
Nature Immunology, 2006, Vol 7, Issue 2, p139
- ISSN
1529-2908
- Publication type
Academic Journal
- DOI
10.1038/ni1294