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We have previously shown that the\n            <jats:italic>Listeria<\/jats:italic>\n            secreted internalin InlC interacts with I\u03baB kinase \u03b1 to interfere with the host immune response (E. Gouin, M. Adib-Conquy, D. Balestrino, M.-A. Nahori, et al., Proc Natl Acad Sci USA, 107:17333\u201317338, 2010,\n            <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"uri\" xlink:href=\"https:\/\/doi.org\/10.1073\/pnas.1007765107\">https:\/\/doi.org\/10.1073\/pnas.1007765107<\/jats:ext-link>\n            ). In the present work, we report that InlC is monoubiquitinated on K\n            <jats:sup>224<\/jats:sup>\n            upon infection of cells and provide evidence that ubiquitinated InlC interacts with and stabilizes the alarmin S100A9, which is a critical regulator of the immune response and inflammatory processes. Additionally, we show that ubiquitination of InlC causes an increase in reactive oxygen species production by neutrophils in mice and restricts\n            <jats:italic>Listeria<\/jats:italic>\n            infection. These findings are the first to identify a posttranscriptional modification of an internalin contributing to host defense.\n          <\/jats:p>","DOI":"10.1128\/mbio.02778-19","type":"journal-article","created":{"date-parts":[[2019,12,16]],"date-time":"2019-12-16T12:54:47Z","timestamp":1576500887000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":17,"title":["Ubiquitination of\n            <i>Listeria<\/i>\n            Virulence Factor InlC Contributes to the Host Response to Infection"],"prefix":"10.1128","volume":"10","author":[{"given":"Edith","family":"Gouin","sequence":"first","affiliation":[{"name":"Institut Pasteur, Unit\u00e9 des Interactions Bact\u00e9ries-Cellules, Paris, France"},{"name":"Inserm, U604, Paris, France"},{"name":"INRA, USC2020, Paris, 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