TRAM is specifically involved in the Toll-like receptor 4–mediated MyD88-independent signaling pathway

By Masahiro Yamamoto, Shintaro Sato, H. Hemmi, Satoshi Uematsu, K. Hoshino, T. Kaisho, O. Takeuchi, K. Takeda, Shizuo Akira. Nature Immunology, 2003

1,179 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology

View Paper: https://www.semanticscholar.org/paper/65121c7bc6762bfbacb70b39362706ca8a2d6fc2

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Citations in the corpus

Phosphoinositide-mediated adaptor recruitment controls Toll-like receptor signaling. (2006, positive): “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).”
Negative regulation of Toll-like receptor-mediated immune responses (2005, background): “The diversity and specificity of TLR function is determined by the selective use of intracellular adaptor molecule”
Inferences, questions and possibilities in Toll-like receptor signalling (2004, background): “82 ), and if LPS is the inciting stimulus, also by way of the TRAM–TRIF–TRAF6 (TNF-receptor-associated factor 6”
Pathogen Recognition and Inflammatory Signaling in Innate Immune Defenses (2009, background): “During TLR3- and TLR4-mediated signaling, TRIF (associated with TRAM in the case of TLR4) (91, 386) is respon-”
NF-κB and the immune response (2006, background): “In TLR4 signaling, TRIF is required for late-phase NF-kB and IRF3 responses, but is not required for activation of JNK (Yamamoto et al., 2003).”
TRIF Licenses Caspase-11-Dependent NLRP3 Inflammasome Activation by Gram-Negative Bacteria (2012, positive): “TRIF is recruited to TLR4 via TRAM or directly to the TIR domain of TLR3 (Kagan et al., 2008; Yamamoto et al., 2003).”
Interferons and viruses: an interplay between induction, signalling, antiviral responses and virus countermeasures. (2008, background): “…and its tyrosine phosphorylation (Sarkar et al., 2004) and recruitment of an adaptor called Toll–interleukin (IL)-1-resistance (TIR) domain-containing adaptor inducing IFN-b (TRIF) (Hoebe et al., 2003; Yamamoto et al., 2003a), as well as phosphatidylinositol 3 (PI3) kinase (Sarkar et al., 2004).”
MyD88: a central player in innate immune signaling (2014, background): “Abbreviations AP-3, adaptor protein 3; DD, death domain; IFNgR, interferon gamma receptor; IRF, interferon regulatory factor; IL, interleukin; INT, intermediate; IRAK, interleukin-1 receptor-associated kinase; LPS, lipopolysaccharide; NFkB, nuclear factor-kappa B; TIR, Toll interleukin-1 receptor; T”