The adaptor molecule TIRAP provides signalling specificity for Toll-like receptors

By T. Horng, G. Barton, R. Flavell, R. Medzhitov. Nature, 2002

908 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology

View Paper: https://www.semanticscholar.org/paper/c04a2c5d59d793a42750c842dfc6e7eb1bc93ab9

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In Cancer Research

1. Shizuo Akira
2. Taro Kawai
3. S. Ghosh
4. K. Takeda
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In Immunology

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8. K. Takeda

Citations in the corpus

• TICAM-1, an adaptor molecule that participates in Toll-like receptor 3–mediated interferon-β induction (2003, background): “However, recently it was shown that cells of TIRAP-deficient mice could still induce IFN-β in response to lipopolysaccharide (LPS), suggesting another adaptor molecule may control this MyD88-independent pathwa”
• Toll-like receptors in antiviral innate immunity (2013, background): “An additional adaptor protein MAL is required for the interaction of TLR2 to MyD88 [159], acting as a linking adaptor via its TIRdomain [9,160].”
• A cell biological view of Toll-like receptor function: regulation through compartmentalization (2009, background): “For example, this model does not clarify why some TLRs require TIRAP to induce a MYD88-dependent signalling response (for example, TLR2 and TLR4) whereas others do not (for example, TLR5, TLR7 and TLR9”
• LPS-TLR4 Signaling to IRF-3/7 and NF-κB Involves the Toll Adapters TRAM and TRIF (2003, background): “, that the Mal/TIRAP dominant negative mutant powerfully inhibited LPS-induced signaling to NF- B (18, 19) and IFN- expression (12, 20), whereas the Mal/TIRAP knockout mouse both retained the ability to induce NF- B (21, 22) and IFN- expression (22).”
• Toll-like receptor function and signaling. (2006, background): “TIR domain–containing adapter protein (TIRAP), also known as MyD88 adaptor–like, was subsequently identified.(41,42) TIRAP-deficient mice showed similar impairment to MyD88-deficient mice in terms of TLR2- and TLR4-induced effects.”
• Innate Immune Pattern Recognition: A Cell Biological Perspective (2015, positive): “CD14 regulates the dendritic cell life cycle after LPS exposure through NFAT activation.”
• How we detect microbes and respond to them: the Toll‐like receptors and their transducers (2003, background): “Targeted deletion of the MAL/Tirap gene yields a phenotype similar to that observed with MyD88 deletion, affecting not only the TLR4 receptor complex but also the TLR2 receptor [61, 62].”
• NF-κB and the immune response (2006, background): “For Oncogene example, MyD88 recruitment to the receptor complex depends upon the TIR-domain containing adapter protein (TIRAP, also known as Mal) (Fitzgerald et al., 2001; Horng et al., 2002; Yamamoto et al., 2002).”
• Endogenous ligands of Toll‐like receptors (2004, background): “Recently, a second TIR-containing adaptor protein, TIR-associated protein (TIRAP)/MyD88-adaptor-like, was identified to be involved in the MyD88-dependent pathways of TLR1/2, TLR2/6, and TLR4 but not other TLRs [29, 30].”
• TLR signaling pathways. (2004, background): “However, generation of TIRAP/Mal knockout mice revealed an unexpected role of TIRAP/Mal in TLR signaling [49,50].”
• TLR4 and CD14 trafficking and its influence on LPS-induced pro-inflammatory signaling (2020, background): “When in the plasma membrane, TLR4 interacts with the first adaptor pair, TIRAP (also called Mal [70]) and MyD88 [71, 72].”
• Pathogen Recognition and Inflammatory Signaling in Innate Immune Defenses (2009, background): “(Mal) (90, 135), TRIF (283, 387), TRIF-related adaptor mol-”