Role of Adaptor TRIF in the MyD88-Independent Toll-Like Receptor Signaling Pathway

By Masahiro Yamamoto, Shintaro Sato, H. Hemmi, K. Hoshino, T. Kaisho, H. Sanjo, O. Takeuchi, Masanaka Sugiyama, M. Okabe, K. Takeda and 1 more. Science, 2003

3,295 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology

View Paper: https://www.semanticscholar.org/paper/8b77e5f5e39401cbb5a82895dc18e7fe90461a88

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Citations in the corpus

Phosphoinositide-mediated adaptor recruitment controls Toll-like receptor signaling. (2006, neutral): “TRAM may function to recruit TRIF to TLR4, but not to TLR3, consistent with the differential requirement for these adaptors for TLR3 and TLR4 signaling (Oshiumi et al., 2003b; Yamamoto et al., 2003b).”
TLR signaling pathways. (2004, background): “In TRIF knockout mice, TLR3-mediated expression of IFNand IFN-inducible genes was impaired [51].”
Toll-like receptors and innate immunity (2006, background): “In addition to proinflammatory signals, some members of the TLR family trigger the induction of type I IFNs.”
Circuitry of nuclear factor κB signaling (2006, background): “The transcription factor IRF3, which is induced by a subset of TLRs, is an obligate coactivator (may not require its cognate DNA-binding site) for a subset of NF-kB-responsive promoters (86, 87).”
Toll-like receptor function and signaling. (2006, methodology): “The function of TIR domain–containing adapter protein inducing IFN-b (TRIF), also called TICAM-1, was revealed by means of analysis on TRIF-deficient mice.(43) This analysis first clarified the MyD88-independent pathway in TLR signaling (Fig 2).”
The adaptor protein MITA links virus-sensing receptors to IRF3 transcription factor activation. (2008, background): “Engagement of TLR3 by dsRNA triggers TRIF (an adaptor of the TLR pathway)-mediated signaling pathways, thereby leading to IRF3 and NF-kB activation (Han et al., 2004; Oshiumi et al., 2003; Yamamoto et al., 2003; Yamamoto et al., 2002).”
Nrf2 is a critical regulator of the innate immune response and survival during experimental sepsis. (2006, methodology): “1 mg glutathione S-transferase–IkBa (1-317) substrate (Santa Cruz Biotech-”
Identification of Oxidative Stress and Toll-like Receptor 4 Signaling as a Key Pathway of Acute Lung Injury (2008, background): “In contrast, trif/ mice ( Yamamoto et al., 2003 ) exhibited markedly improved lung function (Figure 2A), lung pathology (Figure 2B), and lung edema (Figure S3A).”