{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T07:57:42Z","timestamp":1788854262225,"version":"build-2803163510"},"reference-count":57,"publisher":"National Academy of Sciences","issue":"23","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2013,6,4]]},"abstract":"<jats:p>\n                    The regulatory protein PmrA controls expression of lipopolysaccharide (LPS) modification genes in\n                    <jats:italic>Salmonella enterica<\/jats:italic>\n                    serovar Typhimurium, the etiologic agent of human gastroenteritis and murine typhoid fever. PmrA-dependent LPS modifications confer resistance to serum, Fe\n                    <jats:sup>3+<\/jats:sup>\n                    , and several antimicrobial peptides, suggesting that the\n                    <jats:italic>pmrA<\/jats:italic>\n                    gene is required for\n                    <jats:italic>Salmonella<\/jats:italic>\n                    virulence. We now report that, surprisingly, a\n                    <jats:italic>pmrA<\/jats:italic>\n                    null mutant is actually hypervirulent when inoculated i.p. into C3H\/HeN mice. We establish that the PmrA protein binds to the promoter and represses transcription of\n                    <jats:italic>ssrB<\/jats:italic>\n                    , a virulence regulatory gene required for expression of the Spi\/Ssa type three-secretion system inside macrophages. The\n                    <jats:italic>pmrA<\/jats:italic>\n                    mutant displayed heightened expression of SsrB-dependent genes and faster Spi\/Ssa-dependent macrophage killing than wild-type\n                    <jats:italic>Salmonella<\/jats:italic>\n                    . A mutation in the\n                    <jats:italic>ssrB<\/jats:italic>\n                    promoter that abolished repression by the PmrA protein rendered\n                    <jats:italic>Salmonella<\/jats:italic>\n                    as hypervirulent as the\n                    <jats:italic>pmrA<\/jats:italic>\n                    null mutant. The antivirulence function of the PmrA protein may limit the acute phase of\n                    <jats:italic>Salmonella<\/jats:italic>\n                    infection, thereby enhancing pathogen persistence in host tissues.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1303420110","type":"journal-article","created":{"date-parts":[[2013,5,21]],"date-time":"2013-05-21T01:03:59Z","timestamp":1369098239000},"page":"9499-9504","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":37,"title":["The lipopolysaccharide modification regulator PmrA limits\n                    <i>Salmonella<\/i>\n                    virulence by repressing the type three-secretion system Spi\/Ssa"],"prefix":"10.1073","volume":"110","author":[{"given":"Jeongjoon","family":"Choi","sequence":"first","affiliation":[{"name":"Department of Microbial Pathogenesis, Yale School of Medicine, New Haven, CT 06536-0812; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eduardo A.","family":"Groisman","sequence":"additional","affiliation":[{"name":"Department of Microbial Pathogenesis, Yale School of Medicine, New Haven, CT 06536-0812; and"},{"name":"Howard Hughes Medical Institute and"},{"name":"Yale Microbial Diversity Institute, West Haven, CT 06516"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2013,5,20]]},"reference":[{"key":"e_1_3_3_1_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0966-842X(97)01099-8"},{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/nrmicro884"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2958.2002.03070.x"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.73.7.4338-4345.2005"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2958.2006.05512.x"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)00092-1"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1128\/jb.178.17.5092-5099.1996"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.86.13.5054"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/19.8.1861"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1101\/gad.1230804"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1128\/JB.187.21.7407-7416.2005"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.1128\/mr.56.3.395-411.1992"},{"key":"e_1_3_3_13_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2958.2006.05069.x"},{"key":"e_1_3_3_14_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2958.2002.03041.x"},{"key":"e_1_3_3_15_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.ppat.1002454"},{"key":"e_1_3_3_16_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.68.11.6139-6146.2000"},{"key":"e_1_3_3_17_2","doi-asserted-by":"publisher","DOI":"10.1038\/nature05272"},{"key":"e_1_3_3_18_2","doi-asserted-by":"publisher","DOI":"10.1038\/nrmicro1526"},{"key":"e_1_3_3_19_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1462-5822.2002.00234.x"},{"key":"e_1_3_3_20_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2958.2000.01935.x"},{"key":"e_1_3_3_21_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2958.1999.01312.x"},{"key":"e_1_3_3_22_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2958.2007.05800.x"},{"key":"e_1_3_3_23_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.ppat.1000306"},{"key":"e_1_3_3_24_2","doi-asserted-by":"publisher","DOI":"10.1042\/bj3540511"},{"key":"e_1_3_3_25_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.252415599"},{"key":"e_1_3_3_26_2","doi-asserted-by":"publisher","DOI":"10.1128\/AEM.64.6.2240-2246.1998"},{"key":"e_1_3_3_27_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2958.1999.01527.x"},{"key":"e_1_3_3_28_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.00931-09"},{"key":"e_1_3_3_29_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2958.1998.01048.x"},{"key":"e_1_3_3_30_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.67.11.5690-5698.1999"},{"key":"e_1_3_3_31_2","doi-asserted-by":"crossref","first-page":"898","DOI":"10.4049\/jimmunol.114.2_Part_2.898","article-title":"Reticulum cell sarcoma: An effector cell in antibody-dependent cell-mediated immunity","volume":"114","author":"Ralph P","year":"1975","unstructured":"P Ralph, J Prichard, M Cohn, Reticulum cell sarcoma: An effector cell in antibody-dependent cell-mediated immunity. 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