Literature DB >> 25359439

SMOCs: supramolecular organizing centres that control innate immunity.

Jonathan C Kagan1, Venkat Giri Magupalli1, Hao Wu1.   

Abstract

The diverse receptor families of the innate immune system activate signal transduction pathways that are important for host defence, but common themes to explain the operation of these pathways remain undefined. In this Opinion article, we propose--on the basis of recent structural and cell biological studies--the concept of supramolecular organizing centres (SMOCs) as location-specific higher-order signalling complexes in which increased local concentrations of signalling components promote the intrinsically weak allosteric interactions that are required for enzyme activation. We suggest that SMOCs are assembled on various membrane-bound organelles or other intracellular sites, which may assist signal amplification to reach a response threshold and potentially define the specificity of cellular responses that are induced in response to infectious and non-infectious insults.

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Year:  2014        PMID: 25359439      PMCID: PMC4373346          DOI: 10.1038/nri3757

Source DB:  PubMed          Journal:  Nat Rev Immunol        ISSN: 1474-1733            Impact factor:   53.106


  57 in total

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Journal:  Nat Immunol       Date:  2014-06-22       Impact factor: 25.606

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Authors:  Charlotte Odendall; Evelyn Dixit; Fabrizia Stavru; Helene Bierne; Kate M Franz; Ann Fiegen Durbin; Steeve Boulant; Lee Gehrke; Pascale Cossart; Jonathan C Kagan
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  106 in total

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Review 4.  As a toxin dies a prion comes to life: A tentative natural history of the [Het-s] prion.

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Review 6.  Immune signalling by supramolecular assemblies.

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Review 7.  Microbe-inducible trafficking pathways that control Toll-like receptor signaling.

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Review 8.  The Inflammatory Signal Adaptor RIPK3: Functions Beyond Necroptosis.

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9.  Biochemical Isolation of the Myddosome from Murine Macrophages.

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Journal:  Methods Mol Biol       Date:  2018

10.  A Single Bacterial Immune Evasion Strategy Dismantles Both MyD88 and TRIF Signaling Pathways Downstream of TLR4.

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