{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T15:04:20Z","timestamp":1791212660026,"version":"4.1.0"},"reference-count":35,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2016,1,15]],"date-time":"2016-01-15T00:00:00Z","timestamp":1452816000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2016,4]]},"abstract":"<jats:p>\n                    Optineurin (OPTN) is an evolutionary conserved and ubiquitously expressed ubiquitin\u2010binding protein that has been implicated in glaucoma, Paget bone disease, amyotrophic lateral sclerosis, and other neurodegenerative diseases. From in vitro studies, OPTN was shown to suppress TNF\u2010induced NF\u2010\u03baB signaling and virus\u2010induced IRF signaling, and was identified as an autophagy receptor required for the clearance of cytosolic\n                    <jats:italic>Salmonella<\/jats:italic>\n                    upon infection. To assess the in vivo functions of OPTN in inflammation and infection, we generated OPTN\u2010deficient mice. OPTN knockout mice are born with normal Mendelian distribution and develop normally without any signs of spontaneous organ abnormality or inflammation. However, no differences in NF\u2010\u03baB activation could be observed in OPTN knockout mice or fibroblasts derived from these mice upon TNF or LPS treatment. Primary bone marrow\u2010derived macrophages from OPTN\u2010deficient mice had slightly impaired IRF signaling and reduced IFN type I production in response to LPS or poly(I,C). Finally, OPTN\u2010deficient mice were more susceptible to infection with\n                    <jats:italic>Salmonella<\/jats:italic>\n                    , confirming in vivo the importance of OPTN in bacterial clearance.\n                  <\/jats:p>","DOI":"10.1002\/eji.201545863","type":"journal-article","created":{"date-parts":[[2015,12,17]],"date-time":"2015-12-17T10:35:40Z","timestamp":1450348540000},"page":"971-980","source":"Crossref","is-referenced-by-count":86,"title":["Optineurin deficiency in mice is associated with increased sensitivity to\n                    <i>Salmonella<\/i>\n                    but does not affect proinflammatory NF\u2010\u03baB signaling"],"prefix":"10.1002","volume":"46","author":[{"given":"Karolina","family":"Slowicka","sequence":"first","affiliation":[{"name":"Inflammation Research Center Unit of Cellular and Molecular (Patho)physiology  Ghent Belgium"},{"name":"Department of Biomedical Molecular Biology Ghent University  Ghent 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