Unresponsiveness of MyD88-deficient mice to endotoxin.

[1]  S. Akira,et al.  Cutting edge: Toll-like receptor 4 (TLR4)-deficient mice are hyporesponsive to lipopolysaccharide: evidence for TLR4 as the Lps gene product. , 1999, Journal of immunology.

[2]  L. Larivière,et al.  Endotoxin-tolerant Mice Have Mutations in Toll-like Receptor 4 (Tlr4) , 1999, The Journal of experimental medicine.

[3]  P. Ricciardi-Castagnoli,et al.  Defective LPS signaling in C3H/HeJ and C57BL/10ScCr mice: mutations in Tlr4 gene. , 1998, Science.

[4]  M. Rothe,et al.  Human Toll-like Receptor 2 Confers Responsiveness to Bacterial Lipopolysaccharide , 1998, The Journal of experimental medicine.

[5]  S. Gerondakis,et al.  Regulation of an essential innate immune response by the p50 subunit of NF-kappaB. , 1998, The Journal of clinical investigation.

[6]  A. Gurney,et al.  Toll-like receptor-2 mediates lipopolysaccharide-induced cellular signalling , 1998, Nature.

[7]  C. Janeway,et al.  MyD88 is an adaptor protein in the hToll/IL-1 receptor family signaling pathways. , 1998, Molecular cell.

[8]  S. Akira,et al.  Targeted disruption of the MyD88 gene results in loss of IL-1- and IL-18-mediated function. , 1998, Immunity.

[9]  S. Saccani,et al.  The Human Toll Signaling Pathway: Divergence of Nuclear Factor κB and JNK/SAPK Activation Upstream of Tumor Necrosis Factor Receptor–associated Factor 6 (TRAF6) , 1998, The Journal of experimental medicine.

[10]  B. Trask,et al.  Cloning and characterization of two Toll/Interleukin-1 receptor-like genes TIL3 and TIL4: evidence for a multi-gene receptor family in humans. , 1998, Blood.

[11]  L. O’Neill,et al.  Signal transduction pathways activated by the IL‐1 receptor family: ancient signaling machinery in mammals, insects, and plants , 1998, Journal of leukocyte biology.

[12]  F. Martinon,et al.  MyD88, an Adapter Protein Involved in Interleukin-1 Signaling* , 1998, The Journal of Biological Chemistry.

[13]  M. Ikeda,et al.  Interleukin-18 activates the IRAK-TRAF6 pathway in mouse EL-4 cells. , 1998, Biochemical and biophysical research communications.

[14]  S. Akira,et al.  Defective NK cell activity and Th1 response in IL-18-deficient mice. , 1998, Immunity.

[15]  G. Hardiman,et al.  A family of human receptors structurally related to Drosophila Toll. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[16]  Z. Cao,et al.  MyD88: an adapter that recruits IRAK to the IL-1 receptor complex. , 1997, Immunity.

[17]  P. Feng,et al.  IRAK (Pelle) family member IRAK-2 and MyD88 as proximal mediators of IL-1 signaling. , 1997, Science.

[18]  Z. Cao,et al.  Recruitment of IRAK to the interleukin 1 receptor complex requires interleukin 1 receptor accessory protein. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[19]  C. Janeway,et al.  Innate Immunity: The Virtues of a Nonclonal System of Recognition , 1997, Cell.

[20]  P. Morrissey,et al.  Phenotypic and functional characterization of mice that lack the type I receptor for IL-1. , 1997, Journal of immunology.

[21]  C. Janeway,et al.  A human homologue of the Drosophila Toll protein signals activation of adaptive immunity , 1997, Nature.

[22]  G. Shaw,et al.  Membrane binding and enzymatic activation of a Dbl homology domain require the neighboring pleckstrin homology domain. , 1997, Biochemical and biophysical research communications.

[23]  S. Goyert,et al.  CD14-dependent and CD14-independent signaling pathways in murine macrophages from normal and CD14 knockout mice stimulated with lipopolysaccharide or taxol. , 1997, Journal of immunology.

[24]  R. Kamen,et al.  Caspase-1 processes IFN-γ-inducing factor and regulates LPS-induced IFN- γ production , 1997, Nature.

[25]  Klaus Resch,et al.  The Interleukin-1 Receptor Accessory Protein (IL-1RAcP) Is Essential for IL-1-induced Activation of Interleukin-1 Receptor-associated Kinase (IRAK) and Stress-activated Protein Kinases (SAP Kinases)* , 1997, The Journal of Biological Chemistry.

[26]  D. Radzioch,et al.  Secretory Leukocyte Protease Inhibitor: A Macrophage Product Induced by and Antagonistic to Bacterial Lipopolysaccharide , 1997, Cell.

[27]  D. Wallach,et al.  MAP3K-related kinase involved in NF-KB induction by TNF, CD95 and IL-1 , 1997, Nature.

[28]  M. Su,et al.  Activation of Interferon-γ Inducing Factor Mediated by Interleukin-1β Converting Enzyme , 1997, Science.

[29]  Zhaodan Cao,et al.  TRAF6 is a signal transducer for interleukin-1 , 1996, Nature.

[30]  B. Lemaître,et al.  The Dorsoventral Regulatory Gene Cassette spätzle/Toll/cactus Controls the Potent Antifungal Response in Drosophila Adults , 1996, Cell.

[31]  S. Pelech,et al.  Activation of multiple proline-directed kinases by bacterial lipopolysaccharide in murine macrophages. , 1996, Journal of immunology.

[32]  A. DeFranco,et al.  Activation of c-Jun N-terminal kinase in bacterial lipopolysaccharide-stimulated macrophages. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[33]  J. Silver,et al.  Resistance to endotoxin shock and reduced dissemination of gram-negative bacteria in CD14-deficient mice. , 1996, Immunity.

[34]  Z. Cao,et al.  IRAK: A Kinase Associated with the Interleukin-1 Receptor , 1996, Science.

[35]  K. Anderson,et al.  A conserved signaling pathway: the Drosophila toll-dorsal pathway. , 1996, Annual review of cell and developmental biology.

[36]  S. Yamamoto,et al.  Suppression of TNF-alpha mRNA expression in LPS-primed macrophages occurs at the level of nuclear factor-kappa B activation, but not at the level of protein kinase C or CD14 expression. , 1995, Journal of immunology.

[37]  R. Kamen,et al.  Mice deficient in IL-1β-converting enzyme are defective in production of mature IL-1β and resistant to endotoxic shock , 1995, Cell.

[38]  A. Ding,et al.  Macrophages derived from C3H/HeJ (Lpsd ) mice respond to bacterial lipopolysaccharide by activating NF‐χB , 1995, Journal of leukocyte biology.

[39]  R. Ulevitch,et al.  Receptor-dependent mechanisms of cell stimulation by bacterial endotoxin. , 1995, Annual review of immunology.

[40]  H. Ziegler-Heitbrock Molecular mechanism in tolerance to lipopolysaccharide. , 1995, Journal of inflammation.

[41]  T. Yoshida,et al.  LPS induces selective translocation of protein kinase C-beta in LPS-responsive mouse macrophages, but not in LPS-nonresponsive mouse macrophages. , 1994, Journal of immunology.

[42]  L Bibbs,et al.  A MAP kinase targeted by endotoxin and hyperosmolarity in mammalian cells. , 1994, Science.

[43]  I. Fidler,et al.  Protein tyrosine kinase inhibitors decrease induction of nitric oxide synthase activity in lipopolysaccharide-responsive and lipopolysaccharide-nonresponsive murine macrophages. , 1993, Journal of immunology.

[44]  Y. Nakano,et al.  Intracellular protein phosphorylation in murine peritoneal macrophages in response to bacterial lipopolysaccharide (LPS): effects of kinase-inhibitors and LPS-induced tolerance. , 1993, Immunobiology.

[45]  M. Gold,et al.  Bacterial lipopolysaccharide stimulates protein tyrosine phosphorylation in macrophages. , 1991, Proceedings of the National Academy of Sciences of the United States of America.

[46]  R. Ulevitch,et al.  CD14, a receptor for complexes of lipopolysaccharide (LPS) and LPS binding protein. , 1990, Science.

[47]  D. Morrison,et al.  Bacterial endotoxins and host immune responses. , 1979, Advances in immunology.