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      TICAM-1, an adaptor molecule that participates in Toll-like receptor 3-mediated interferon-beta induction.

      Nature immunology
      Adaptor Proteins, Signal Transducing, Adaptor Proteins, Vesicular Transport, genetics, immunology, metabolism, Amino Acid Sequence, Animals, Antigens, Differentiation, Binding Sites, Cell Line, Cloning, Molecular, DNA-Binding Proteins, Drosophila Proteins, Female, Gene Silencing, Humans, Immunity, Cellular, Interferon Regulatory Factor-3, Interferon-beta, biosynthesis, Male, Membrane Glycoproteins, chemistry, Mice, Molecular Sequence Data, Myeloid Differentiation Factor 88, NF-kappa B, Pregnancy, Protein Structure, Tertiary, RNA, Double-Stranded, Receptors, Cell Surface, Receptors, Immunologic, Receptors, Interleukin-1, Sequence Homology, Amino Acid, Signal Transduction, Tissue Distribution, Toll-Like Receptor 3, Toll-Like Receptors, Transcription Factor AP-1, Transcription Factors

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          Abstract

          Human Toll-like receptor (TLR) 3 recognizes double-stranded (ds) RNA and induces production of interferon (IFN)-beta independent of the adaptor molecules MyD88 and TIRAP. Thus, another adaptor must exist that preferentially mediates TLR3-dependent production of IFN-beta. We have identified an alternative adaptor, designated Toll-interleukin 1 receptor domain (TIR)-containing adaptor molecule (TICAM)-1, that can physically bind the TIR domain of TLR3 and activate the IFN-beta promoter in response to poly(I):poly(C). Thus, dsRNA-TLR3-dependent production of IFN-beta is mediated mainly by TICAM-1. This TICAM-1-dependent pathway may have a role in other TLR-IFN-beta pathways, which form part of the MyD88-independent cellular immune response.

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