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Toll/Interleukin-1 receptor

Martin, M.U. and Wesche, H., Summary and comparison of the signaling mechanisms of the Toll/interleukin-1 receptor family, Biochim. Biophys. Acta, 1592(3), 265, 2002. [Pg.87]

Dunne, A., Ejdeback, M., Ludidi, P.L., O Neill, L.A., Gay, N.J. Structural complementarity of Toll/interleukin-1 receptor domains in Toll-like receptors and the adaptors Mai and MyD88. J Biol Chem 278 (2003) 41443-41451. [Pg.166]

O Neill, L., The Toll/interleukin-1 receptor domain a molecular switch for inflammation and host defense. Biochem Soc Trans 28 (2000) 557-563. [Pg.183]

Xu Y, Tao X, Shen B, Horng T, Medzhitov R, et al. 2000. Structural basis for signal transduction by the Toll/interleukin-1 receptor domains. Nature 408 111-15... [Pg.627]

Figure 33.1 Toll-like receptor. Each receptor comprises a set of 18 or more leucine-rich repeat sequences, followed by a cysteine-rich domain, a single transmembrane helix, and a TIR (Toll-interleukin 1 receptor) domain that functions in signal transduction. Figure 33.1 Toll-like receptor. Each receptor comprises a set of 18 or more leucine-rich repeat sequences, followed by a cysteine-rich domain, a single transmembrane helix, and a TIR (Toll-interleukin 1 receptor) domain that functions in signal transduction.
Cirl C, Wieser A, Yadav M et al. Subversion of Toll-like receptor signaling by a unique family of bacterial Toll/interleukin-1 receptor domain-containing proteins. Nat Med 2008 14(4) 399-406. [Pg.62]

TLRs are transmembrane receptors comprising an extracellular leucine-rich repeat and a cytoplasmic Toll/interleukin-1 receptor (TIR) domain, which are connected through a transmembrane domain [4]. The TIR domain is structurally homologous... [Pg.63]

In conclusion, IFNs have proven to be invaluable tools in the fight against chronic viral hepatitis. In these indications, their antiviral properties play a major role and it remains unclear whether their immunomodulatory properties are also important. Disappointing results obtained with purely immunomodulatory molecules, such as interleukins or Toll-like receptor agonists suggest that, if immunomodulation plays any role, potent inhibition of viral replication is also needed. The role of IFNs in the treatment of viral infections other than hepatitis B and C remains elusive. [Pg.230]

Suzuki, N. et al. Severe impairment of interleukin-1 and Toll-like receptor signalling in mice lacking IRAK-4. Nature 416, 750, 2002. [Pg.304]

Uematsu, S., et al., Interleukin-1 receptor-associated kinase-1 plays an essential role for Toll-like receptor (TLR)7- and TLR9-mediated interferon- alpha induction, J. Exp. Med. 201, 6, 915, 2005. [Pg.324]

Crustacea Arthropods, Crustaceans, Insects Lectins, PO, Leucine rich repeats, Toll, Tol interleukin receptors, AMPs, complement... [Pg.369]

Endotoxicity results from the interaction of a bacterial cell envelope component (e.g., LPS or PG with a cell surface receptor constituting part of the nonspecific immune system, (i.e., a toll-like receptor on white blood cells). This results in the production of cytokines [e.g., interleukin 1 (IL-1) or tumor necrosis factor (TNF)] as part of an intracellular enzyme cascade which can cause severe tissue injury. Bioassays or immunoassays can be used to detect such reactions respectively. As noted above the most widely used bioassay is the LAL assay. A lysate of amoebo-cytes of the horseshoe crab (Limulus) contains an enzymatic clotting cascade which is activated by extremely low levels of LPS (nanogram levels or lower). There are variants of this assay that can detect PG, but they are not as widely used. As noted above, other bioassays employ cultured cell lines that respond to LPS or PG, respectively. Unfortunately bioassays are highly amenable to false positives (from the presence of cross-reactive substances) or false negatives from inhibition (by contaminants present in the sample) [10]. A detailed discussion of these assays is beyond the scope of this chapter and has been reviewed elsewhere [1]. [Pg.535]

Koziczak-Holbro M, Joyce C, Gluk A, Kinzel B, et al. 2007. IRAK-4 kinase activity is required for interleukin-1 (IL-1) receptor- and toll-like receptor-7 mediated signaling and gene expression. J Biol Chem. 282 13552-13560. [Pg.84]

Dunne, A. and O Neill, L.A., The interleukin-1 receptor/Toll-like receptor superfamily Signal transduction during inflammation and host defense, Sci STKE, 25, 2003(171), 2003. [Pg.87]

Burns, K., lanssens, S., Brissoni, B., Olivos, N., Beyaert, R., Tschopp, J. Inhibition of interleukin 1 receptor/Toll-like receptor signaling through the alternatively spliced, short form of MyD88 is due to its failure to recruit IRAK-4.1 Exp Med, 197 (2003) 263-268. [Pg.166]

Conze, D.B., Wu, C.J., Thomas, J.A., Landstrom, A., Ashwell, J.D. Lys63-linked polyubiquitination of IRAK-1 is required for interleukin-1 receptor- and toll-like receptor-mediated NF-kappaB activation. Mol Cell Biol 28 (2008) 3538-3547. [Pg.166]

Suzuki, N., Suzuki, S., Duncan, G.S., Millar, D.G., Wada, T., Mirtsos, C., Takada, H.. et al. Severe impairment of interleukin-1 and Toll-like receptor signalling in mice lacking IRAK-4. Nature 416 (2002) 750-756. [Pg.170]

Wald, D., Qin, J., Zhao, Z., Qian, Y., Naramura, M., Tian, L., Towne, J., et al. SIGIRR, a negative regulator of Toll-like receptor-interleukin 1 receptor signaling, Nat Immunol 4 (2003) 920-927. [Pg.170]

Gobert, A.P., Bambou, J.-C., Werts, C., Balloy, V., Chignard, M., Moran, A.P., and Ferrero, R.L. Helicobacter pylori heat shock protein 60 mediates interleukin-6 production by macrophages via a Toll-like receptor (TLR)-2-, TLR-4-, and myeloid differentiation factor 88-independent mechanism. J Biol Chem 279 (2004) 245-250. [Pg.233]

Machida K, Cheng KT, Sung VM, Levine AM, Foung, S and Lai MM Hepatitis C virus induces toll-like receptor 4 expression, leading to enhanced production of beta interferon and interleukin-6. / Virol 2006 80(2) 866-74. [Pg.747]

Walton, K.A. et al. Receptors involved in the oxidized l-pahnitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine-mediated synthesis of interleukin-8. A role for Toll-like receptor 4 and a glycosylphosphatidyhnositol-anchored protein. J. Biol Chem. 278 (2003b) 29661-6. [Pg.350]

Erridge, C., Webb, D. J., and Spickett, C. M. 2007. Toll-like receptor 4 signalling is neither sufficient nor required for oxidised phospholipid mediated induction of interleukin-8 expression. 193, 77-85. [Pg.17]


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See also in sourсe #XX -- [ Pg.216 ]




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Interleukine

Interleukines

Interleukins interleukin-1 receptor

Intracellular toll/interleukin-1 receptor

Tolls

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