{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T19:19:04Z","timestamp":1792696744074,"version":"4.5.0"},"reference-count":35,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"6151","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Science"],"published-print":{"date-parts":[[2013,9,13]]},"abstract":"<jats:title>Move Over, TLR4<\/jats:title>\n                  <jats:p>\n                    The innate immune system senses bacterial lipopolysaccharide (LPS) through Toll-like receptor 4 (TLR4) (see the Perspective by\n                    <jats:bold>\n                      <jats:related-article xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" issue=\"6151\" page=\"1184\" related-article-type=\"in-this-issue\" vol=\"341\" xlink:href=\"10.1126\/science.1243939\">Kagan<\/jats:related-article>\n                    <\/jats:bold>\n                    ). However,\n                    <jats:bold>\n                      Kayagaki\n                      <jats:italic>et al.<\/jats:italic>\n                    <\/jats:bold>\n                    (p\n                    <jats:related-article xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" issue=\"6151\" page=\"1246\" related-article-type=\"in-this-issue\" vol=\"341\" xlink:href=\"10.1126\/science.1240248\">1246<\/jats:related-article>\n                    , published online 25 July) and\n                    <jats:bold>\n                      Hagar\n                      <jats:italic>et al.<\/jats:italic>\n                    <\/jats:bold>\n                    (p.\n                    <jats:related-article xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" issue=\"6151\" page=\"1250\" related-article-type=\"in-this-issue\" vol=\"341\" xlink:href=\"10.1126\/science.1240988\">1250<\/jats:related-article>\n                    ) report that the hexa-acyl lipid A component of LPS from Gramnegative bacteria is able to access the cytoplasm and activate caspase-11 to signal immune responses independently of TLR4. Mice that lack caspase-11 are resistant to LPS-induced lethality, even in the presence of TLR4.\n                  <\/jats:p>","DOI":"10.1126\/science.1240248","type":"journal-article","created":{"date-parts":[[2013,7,26]],"date-time":"2013-07-26T07:55:01Z","timestamp":1374825301000},"page":"1246-1249","source":"Crossref","is-referenced-by-count":1465,"title":["Noncanonical Inflammasome Activation by Intracellular LPS Independent of TLR4"],"prefix":"10.1126","volume":"341","author":[{"given":"Nobuhiko","family":"Kayagaki","sequence":"first","affiliation":[{"name":"Department of Physiological Chemistry, Genentech, South San Francisco, CA 94080, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael T.","family":"Wong","sequence":"additional","affiliation":[{"name":"Department of Physiological Chemistry, Genentech, South San Francisco, CA 94080, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Irma B.","family":"Stowe","sequence":"additional","affiliation":[{"name":"Department of Physiological Chemistry, Genentech, South San Francisco, CA 94080, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sree Ranjani","family":"Ramani","sequence":"additional","affiliation":[{"name":"Department of Protein Chemistry, Genentech, South San Francisco, CA 94080, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lino C.","family":"Gonzalez","sequence":"additional","affiliation":[{"name":"Department of Protein Chemistry, Genentech, South San Francisco, CA 94080, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sachiko","family":"Akashi-Takamura","sequence":"additional","affiliation":[{"name":"Division of Innate Immunity, Department of Microbiology and Immunology, Laboratory of Innate Immunity, Center for Experimental Medicine and Systems Biology, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, 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