{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T13:56:53Z","timestamp":1790776613137,"version":"4.1.0"},"reference-count":33,"publisher":"American Society for Microbiology","issue":"4","license":[{"start":{"date-parts":[[2017,4,1]],"date-time":"2017-04-01T00:00:00Z","timestamp":1491004800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100000060","name":"HHS | NIH | National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["AI120489"],"award-info":[{"award-number":["AI120489"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"HHS | NIH | National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["AI109316"],"award-info":[{"award-number":["AI109316"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2017,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Bacteria have developed capacities to deal with different stresses and adapt to different environmental niches. The human pathogen\n                    <jats:named-content content-type=\"genus-species\">Vibrio cholerae<\/jats:named-content>\n                    , the causative agent of the severe diarrheal disease cholera, utilizes the transcriptional regulator OxyR to activate genes related to oxidative stress resistance, including peroxiredoxin PrxA, in response to hydrogen peroxide. In this study, we identified another OxyR homolog in\n                    <jats:named-content content-type=\"genus-species\">V. cholerae<\/jats:named-content>\n                    , which we named OxyR2, and we renamed the previous OxyR OxyR1. We found that OxyR2 is required to activate its divergently transcribed gene\n                    <jats:italic>ahpC<\/jats:italic>\n                    , encoding an alkylhydroperoxide reductase, independently of H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    . A conserved cysteine residue in OxyR2 is critical for this function. Mutation of either\n                    <jats:italic>oxyR2<\/jats:italic>\n                    or\n                    <jats:italic>ahpC<\/jats:italic>\n                    rendered\n                    <jats:named-content content-type=\"genus-species\">V. cholerae<\/jats:named-content>\n                    more resistant to H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    . RNA sequencing analyses indicated that OxyR1-activated oxidative stress-resistant genes were highly expressed in\n                    <jats:italic>oxyR2<\/jats:italic>\n                    mutants even in the absence of H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    . Further genetic analyses suggest that OxyR2-activated AhpC modulates OxyR1 activity by maintaining low intracellular concentrations of H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    . Furthermore, we showed that \u0394\n                    <jats:italic>oxyR2<\/jats:italic>\n                    and \u0394\n                    <jats:italic>ahpC<\/jats:italic>\n                    mutants were less fit when anaerobically grown bacteria were exposed to low levels of H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    or incubated in seawater. These results suggest that OxyR2 and AhpC play important roles in the\n                    <jats:named-content content-type=\"genus-species\">V. cholerae<\/jats:named-content>\n                    oxidative stress response.\n                  <\/jats:p>","DOI":"10.1128\/iai.00929-16","type":"journal-article","created":{"date-parts":[[2017,1,30]],"date-time":"2017-01-30T21:20:26Z","timestamp":1485811226000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":30,"title":["OxyR2 Modulates OxyR1 Activity and Vibrio cholerae Oxidative Stress Response"],"prefix":"10.1128","volume":"85","author":[{"given":"Hui","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Microbiology, Nanjing Agricultural University, Nanjing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nawar","family":"Naseer","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yaran","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Nanjing Agricultural University, Nanjing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anthony Y.","family":"Zhu","sequence":"additional","affiliation":[{"name":"Harriton High School, Bryn Mawr, Pennsylvania, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xuewen","family":"Kuai","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Nanjing Agricultural University, Nanjing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nirupa","family":"Galagedera","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhi","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Biotechnology, Huazhong University of Science and Technology, Wuhan, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jun","family":"Zhu","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(03)15328-7"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.01094-07"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1348-0421.2002.tb02659.x"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1038\/nrmicro2204"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.biochem.77.061606.161055"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.68.040104.110001"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbagen.2003.10.016"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1128\/CDLI.9.2.221-229.2002"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.02765-14"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.abb.2012.04.014"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.1099\/mic.0.2008\/022772-0"},{"key":"e_1_3_3_13_2","doi-asserted-by":"publisher","DOI":"10.1038\/nsmb856"},{"key":"e_1_3_3_14_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(02)00723-7"},{"key":"e_1_3_3_15_2","doi-asserted-by":"publisher","DOI":"10.1126\/stke.2002.157.pe46"},{"key":"e_1_3_3_16_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0053383"},{"key":"e_1_3_3_17_2","article-title":"OxyR-activated expression of Dps is important for Vibrio cholerae oxidative stress resistance and pathogenesis","author":"Xia X","unstructured":"Xia X Larios-Valencia J Liu Z Xiang F Kan B Wang H Zhu J . OxyR-activated expression of Dps is important for Vibrio cholerae oxidative stress resistance and pathogenesis. 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