Specificity in Toll-like receptor signalling through distinct effector functions of TRAF3 and TRAF6

By Hans Häcker, V. Redecke, I. Kratchmarova, L. Hsu, Gang G. Wang, M. Kamps, E. Raz, H. Wagner, G. Häcker, Matthias Mann and 1 more. Nature, 2006

1,014 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology

View Paper: https://www.semanticscholar.org/paper/4f7a192d8759561cd09a546c6ca19aeeff9eaef9

How researchers see this paper

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In Cancer Research

1. Shizuo Akira
2. T. Mogensen
3. M. Karin
4. G. Barton
5. T. Kaisho
6. O. Takeuchi
7. Minghua Wu
8. Danyang Li

In Immunology

1. Shizuo Akira
2. T. Mogensen
3. O. Takeuchi
4. R. Medzhitov
5. M. Karin
6. Taro Kawai
7. R. Randall
8. S. Goodbourn

Citations in the corpus

• Immune signaling by RIG-I-like receptors (2011, background): “In addition, TNFR-associated factor 3 (TRAF3), a K63-linked E3 ubiquitin ligase that is essential for regulating virus-induced IRF3 activation (Häcker et al., 2006; Oganesyan et al., 2006), was found to regulate IFN but not inflammatory cytokine production during virus infection.”
• MyD88: a central player in innate immune signaling (2014, background): “Two TNF receptor-associated factors (TRAFs)— TRAF3 and TRAF6—can be activated by IRAK family members and lead to the production of type I IFN or proinflammatory cytokines, respectively [51,52].”
• Pattern recognition receptors in health and diseases (2021, background): “TRAF6 is degraded due to its own ubiquitination.(262,263) The TAK1–TAB1–TAB4 complex activates the IκB kinase (IKK) complex through phosphorylation.”
• Innate immunity gone awry: linking microbial infections to chronic inflammation and cancer. (2006, background): “AC = apoptotic cell; IC = immune complex with nucleic acid; SR = scavenger receptor; TLR = Toll-like receptor; Hsp = heat-shock protein; RON = recepteur d’origine nantis; CD200L = CD200 ligand; HMG-B1 = high mobility group box 1 protein (chromatin component); RAGE = receptor for advanced glycation p”
• Toll-like receptor function and signaling. (2006, background): “Interestingly, TRAF-3 deficiency also led to similar defective phenotype in TLR7/9 signaling to that of IRF-7– or IRAK-1–deficient mice in terms of selective impairment in type I IFN induction.(53,54) TRAF3 seems to function as a molecular rudder to steer into type I IFN induction.”
• Coronavirus infections and immune responses (2020, background): “In addition to activating NF‐kB, TRIF‐dependent pathways, they also activate IRF3 and interferon‐β.(10,11)”
• Toll-like receptors in antiviral innate immunity (2013, background): “This may be explained by the proposal that TRAF3, a cytosolic adaptor essential for IFN induction via TLR and RLR signaling pathways [40,41], does not have ready access to plasma membrane signaling complexes [42].”
• Innate Immune Pattern Recognition: A Cell Biological Perspective (2015, neutral): “TRAF3 interacts with TANK or TANK-related proteins (153) to recruit the kinases TBK1 and IKKε for IRF3 activation, thus regulating type I IFN production (154–156).”