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10.1038/s41598-017-05230-2 http://scihub22266oqcxt.onion/10.1038/s41598-017-05230-2 C5506048!5506048 !28698597     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28698597 &cmd=llinks): Failed to open stream: HTTP request failed! 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Selenoprotein MsrB1 promotes anti-inflammatory cytokine gene expression in macrophages and controls immune response in vivo |pdf=|usr=}}{{28698597 }} gab.com Text Selenoprotein MsrB1 promotes anti-inflammatory cytokine gene expression in macrophages and controls immune response in vivo JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28698597 #FOAvip Post-translational redox modification of methionine residues often triggers a change in protein function. Emerging evidence points to this reversible protein modification being an important regulatory mechanism under various physiological conditions. Reduction of oxidized methionine residues is catalyzed by methionine sulfoxide reductases (Msrs). Here, we show that one of these enzymes, a selenium-containing MsrB1, is highly expressed in immune-activated macrophages and contributes to shaping cellular and organismal immune responses. In particular, lipopolysaccharide (LPS) induces expression of MsrB1, but not other Msrs. Genetic ablation of MsrB1 did not preclude LPS-induced intracellular signaling in macrophages, but resulted in attenuated induction of anti-inflammatory cytokines, such as interleukin (IL)-10 and the IL-1 receptor antagonist. This anomaly was associated with excessive pro-inflammatory cytokine production as well as an increase in acute tissue inflammation in mice. Together, our findings suggest that MsrB1 controls immune responses by promoting anti-inflammatory cytokine expression in macrophages. MsrB1-dependent reduction of oxidized methionine in proteins may be a heretofore unrecognized regulatory event underlying immunity and inflammatory disease, and a novel target for clinical applications. Twit Text FOAVip Selenoprotein MsrB1 promotes anti-inflammatory cytokine gene expression in macrophages and controls immune response in vivo ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28698597 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28698597 #FOAvip English Wikipedia <ref>{{Cite pmid|28698597 }}</ref> Selenoprotein MsrB1 promotes anti-inflammatory cytokine gene expression in macrophages and controls immune response in vivo #MMPMID28698597 Lee BC ; Lee SG ; Choo MK ; Kim JH ; Lee HM ; Kim S ; Fomenko DE ; Kim HY ; Park JM ; Gladyshev VN Sci Rep 2017[Jul]; 7 (1 ): 5119 PMID28698597 show ga Post-translational redox modification of methionine residues often triggers a change in protein function. Emerging evidence points to this reversible protein modification being an important regulatory mechanism under various physiological conditions. Reduction of oxidized methionine residues is catalyzed by methionine sulfoxide reductases (Msrs). Here, we show that one of these enzymes, a selenium-containing MsrB1, is highly expressed in immune-activated macrophages and contributes to shaping cellular and organismal immune responses. In particular, lipopolysaccharide (LPS) induces expression of MsrB1, but not other Msrs. Genetic ablation of MsrB1 did not preclude LPS-induced intracellular signaling in macrophages, but resulted in attenuated induction of anti-inflammatory cytokines, such as interleukin (IL)-10 and the IL-1 receptor antagonist. This anomaly was associated with excessive pro-inflammatory cytokine production as well as an increase in acute tissue inflammation in mice. Together, our findings suggest that MsrB1 controls immune responses by promoting anti-inflammatory cytokine expression in macrophages. MsrB1-dependent reduction of oxidized methionine in proteins may be a heretofore unrecognized regulatory event underlying immunity and inflammatory disease, and a novel target for clinical applications. |Animals [MESH] |Cells, Cultured [MESH] |Female [MESH] |Gene Expression Regulation/drug effects [MESH] |Interleukin 1 Receptor Antagonist Protein/genetics [MESH] |Interleukin-10/genetics [MESH] |Lipopolysaccharides/*adverse effects [MESH] |Macrophages/cytology/*drug effects/metabolism [MESH] |Methionine Sulfoxide Reductases/genetics/*metabolism [MESH] |Mice [MESH] |Phorbol Esters/*adverse effects [MESH] |Signal Transduction [MESH]Selenoprotein MsrB1 promotes anti-inflammatory cytokine gene expressio(epmc).pdf DeepDyve Pubget Overpricing