{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T22:45:53Z","timestamp":1793227553721,"version":"4.5.0"},"reference-count":35,"publisher":"American Society for Microbiology","issue":"1","license":[{"start":{"date-parts":[[2001,1,1]],"date-time":"2001-01-01T00:00:00Z","timestamp":978307200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Antimicrob Agents Chemother"],"published-print":{"date-parts":[[2001,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            The\n            <jats:italic>soxRS<\/jats:italic>\n            regulon is activated by redox-cycling drugs such as paraquat and by nitric oxide. The &gt;15 genes of this system provide resistance to both oxidants and multiple antibiotics. An association between clinical quinolone resistance and elevated expression of the\n            <jats:italic>soxRS<\/jats:italic>\n            regulon has been observed in\n            <jats:italic>Escherichia coli<\/jats:italic>\n            , but this association has not been explored for other enteropathogenic bacteria. Here we describe a\n            <jats:italic>soxRS<\/jats:italic>\n            -constitutive mutation in a clinical strain of\n            <jats:italic>Salmonella enterica<\/jats:italic>\n            (serovar Typhimurium) that arose with the development of resistance to quinolones during treatment. The elevated quinolone resistance in this strain derived from a point mutation in the\n            <jats:italic>soxR<\/jats:italic>\n            gene and could be suppressed in\n            <jats:italic>trans<\/jats:italic>\n            by multicopy wild-type\n            <jats:italic>soxRS<\/jats:italic>\n            . Multiple-antibiotic resistance was also transferred to a laboratory strain of\n            <jats:italic>S. enterica<\/jats:italic>\n            by introducing the cloned mutant\n            <jats:italic>soxR<\/jats:italic>\n            gene from the clinical strain. The results show that constitutive expression of\n            <jats:italic>soxRS<\/jats:italic>\n            can contribute to antibiotic resistance in clinically relevant\n            <jats:italic>S. enterica.<\/jats:italic>\n          <\/jats:p>","DOI":"10.1128\/aac.45.1.38-43.2001","type":"journal-article","created":{"date-parts":[[2002,7,27]],"date-time":"2002-07-27T10:06:42Z","timestamp":1027764402000},"page":"38-43","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":93,"title":["A\n            <i>soxRS<\/i>\n            -Constitutive Mutation Contributing to Antibiotic Resistance in a Clinical Isolate of\n            <i>Salmonella enterica<\/i>\n            (Serovar Typhimurium)"],"prefix":"10.1128","volume":"45","author":[{"given":"Anastasia","family":"Koutsolioutsou","sequence":"first","affiliation":[{"name":"<!--label omitted: 1-->Department of Cancer Cell Biology and Division of Biological Sciences, Harvard School of Public Health, Boston, Massachusetts 02115,1 and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elizabeth A.","family":"Martins","sequence":"additional","affiliation":[{"name":"<!--label omitted: 1-->Department of Cancer Cell Biology and Division of Biological Sciences, Harvard School of Public Health, Boston, Massachusetts 02115,1 and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D. G.","family":"White","sequence":"additional","affiliation":[{"name":"<!--label omitted: 2-->Center for Adaptation Genetics and Drug Resistance, Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts 021112"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S. B.","family":"Levy","sequence":"additional","affiliation":[{"name":"<!--label omitted: 2-->Center for Adaptation Genetics and Drug Resistance, Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts 021112"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bruce","family":"Demple","sequence":"additional","affiliation":[{"name":"<!--label omitted: 1-->Department of Cancer Cell Biology and Division of Biological Sciences, Harvard School of Public Health, Boston, Massachusetts 02115,1 and"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.41.10.2067"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/JB.180.4.938-944.1998"},{"key":"e_1_3_2_4_2","unstructured":"Ausubel\n              F. M.\n              Brent\n              R.\n              Kingston\n              R. 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S.\n          1996\n          435\n          452\n          Landes Co.\n          Austin Tex","DOI":"10.1007\/978-1-4684-8601-8_21"},{"key":"e_1_3_2_18_2","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1994.tb06243.x"},{"key":"e_1_3_2_19_2","doi-asserted-by":"crossref","first-page":"121","DOI":"10.1016\/S0092-8674(00)81864-4","article-title":"Redox signal transduction: mutations shifting [2Fe-2S] centers of the SoxR sensor-regulator to the oxidized form.","volume":"88","author":"Hidalgo E.","year":"1997","unstructured":"Hidalgo E. Ding H. Demple B. Redox signal transduction: mutations shifting [2Fe-2S] centers of the SoxR sensor-regulator to the oxidized form. 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