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  • Death, TIR, and RHIM: Self-assembling domains involved in innate immunity and cell-death signaling

    Author(s)
    Nanson, Jeffrey D
    Kobe, Bostjan
    Ve, Thomas
    Griffith University Author(s)
    Ve, Thomas
    Year published
    2019
    Metadata
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    Abstract
    The innate immune system consists of pattern recognition receptors (PRRs) that detect pathogen‐ and endogenous danger‐associated molecular patterns (PAMPs and DAMPs), initiating signaling pathways that lead to the induction of cytokine expression, processing of pro‐inflammatory cytokines, and induction of cell‐death responses. An emerging concept in these pathways and associated processes is signaling by cooperative assembly formation (SCAF), which involves formation of higher order oligomeric complexes, and enables rapid and strongly amplified signaling responses to minute amounts of stimulus. Many of these signalosomes ...
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    The innate immune system consists of pattern recognition receptors (PRRs) that detect pathogen‐ and endogenous danger‐associated molecular patterns (PAMPs and DAMPs), initiating signaling pathways that lead to the induction of cytokine expression, processing of pro‐inflammatory cytokines, and induction of cell‐death responses. An emerging concept in these pathways and associated processes is signaling by cooperative assembly formation (SCAF), which involves formation of higher order oligomeric complexes, and enables rapid and strongly amplified signaling responses to minute amounts of stimulus. Many of these signalosomes assemble through homotypic interactions of members of the death‐fold (DF) superfamily, Toll/IL‐1 receptor (TIR) domains, or the RIP homotypic interaction motifs (RHIM). We review the current understanding of the structure and function of these domains and their molecular interactions with a particular focus on higher order assemblies.
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    Journal Title
    JOURNAL OF LEUKOCYTE BIOLOGY
    Volume
    105
    Issue
    2
    DOI
    https://doi.org/10.1002/JLB.MR0318-123R
    Subject
    Biochemistry and cell biology
    Immunology
    Publication URI
    http://hdl.handle.net/10072/385826
    Collection
    • Journal articles

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