- The Transmembrane Adaptor Protein SCIMP Facilitates Sustained Dectin-…
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The Transmembrane Adaptor Protein SCIMP Facilitates Sustained Dectin-1 Signaling in Dendritic Cells

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    SYSNO ASEP0472003
    Document TypeJ - Journal Article
    R&D Document TypeJournal Article
    Subsidiary JČlánek ve WOS
    TitleThe Transmembrane Adaptor Protein SCIMP Facilitates Sustained Dectin-1 Signaling in Dendritic Cells
    Author(s) Králová, Jarmila (UMG-J)
    Fabišik, Matěj (UMG-J)
    Pokorná, Jana (UMG-J)
    Skopcová, Tereza (UMG-J)
    Malissen, B. (FR)
    Brdička, Tomáš (UMG-J) RID, ORCID
    Number of authors6
    Source TitleJournal of Biological Chemistry. - : Elsevier - ISSN 0021-9258
    Roč. 291, č. 32 (2016), s. 16530-16540
    Number of pages11 s.
    Languageeng - English
    CountryUS - United States
    Keywordsbeta-glucan receptor ; c-type lectin ; toll-like receptors ; fungal-infections ; antifungal immunity ; pattern-recognition ; candida-albicans ; erk activation ; mice ; innate
    Subject RIVEB - Genetics ; Molecular Biology
    R&D ProjectsGAP302/12/1712 GA ČR - Czech Science Foundation (CSF)
    Institutional supportUMG-J - RVO:68378050
    UT WOS000380826700013
    DOI https://doi.org/10.1074/jbc.M116.717157
    AnnotationTransmembrane adaptor proteins are molecules specialized in recruiting cytoplasmic proteins to the proximity of the cell membrane as part of the signal transduction process. A member of this family, SLP65/SLP76, Csk-interacting membrane protein (SCIMP), recruits a complex of SLP65/SLP76 and Grb2 adaptor proteins, known to be involved in the activation of PLC gamma 1/2, Ras, and other pathways. SCIMP expression is restricted to antigen-presenting cells. In a previous cell line-based study, it was shown that, in B cells, SCIMP contributes to the reverse signaling in the immunological synapse, downstream of MHCII glycoproteins. There it mainly facilitates the activation of ERK MAP kinases. However, its importance for MHCII glycoprotein-dependent ERK signaling in primary B cells has not been analyzed. Moreover, its role in macrophages and dendritic cells has remained largely unknown. Here we present the results of our analysis of SCIMP-deficient mice. In these mice, we did not observe any defects in B cell signaling and B cell-dependent responses. On the other hand, we found that, in dendritic cells and macrophages, SCIMP expression is up-regulated after exposure to GM-CSF or the Dectin-1 agonist zymosan. Moreover, we found that SCIMP is strongly phosphorylated after Dectin-1 stimulation and that it participates in signal transduction downstream of this important pattern recognition receptor. Our analysis of SCIMP-deficient dendritic cells revealed that SCIMP specifically contributes to sustaining long-term MAP kinase signaling and cytokine production downstream of Dectin-1 because of an increased expression and sustained phosphorylation lasting at least 24 h after signal initiation.
    WorkplaceInstitute of Molecular Genetics
    ContactNikol Škňouřilová, nikol.sknourilova@img.cas.cz, Tel.: 241 063 217
    Year of Publishing2017
Number of the records: 1  

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