{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,30]],"date-time":"2026-10-30T21:25:03Z","timestamp":1793395503123,"version":"4.5.0"},"reference-count":51,"publisher":"American Society for Microbiology","issue":"3","license":[{"start":{"date-parts":[[2003,3,1]],"date-time":"2003-03-01T00:00:00Z","timestamp":1046476800000},"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":[[2003,3]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            We found an increased abundance of\n            <jats:italic>pbpB<\/jats:italic>\n            -specific transcripts in vancomycin intermediate-resistant\n            <jats:italic>Staphylococcus aureus<\/jats:italic>\n            (VISA) isolates compared with that found in paired, genetically identical, susceptible isolates. This difference in expression cannot be explained by differences in the\n            <jats:italic>pbpB<\/jats:italic>\n            promoter sequence. Since the factors controlling\n            <jats:italic>pbpB<\/jats:italic>\n            gene expression have remained largely unexplored, various conditions that might affect\n            <jats:italic>pbpB<\/jats:italic>\n            transcript abundance were examined. In both vancomycin-susceptible and VISA strains,\n            <jats:italic>pbpB<\/jats:italic>\n            expression varied with the growth phase, with the highest abundance of\n            <jats:italic>pbpB<\/jats:italic>\n            -specific transcripts detected during mid-log phase. Interestingly, both vancomycin and oxacillin were able to induce\n            <jats:italic>pbpB<\/jats:italic>\n            transcription above a constitutive level. When vancomycin was absent, one of the three\n            <jats:italic>pbpB<\/jats:italic>\n            -specific transcripts that were usually faintly detected in non-VISA strains was more readily detected in VISA strains during mid-log but not stationary phase. This transcript was enhanced in non-VISA strains by vancomycin induction. Gel shift assays indicated that an increased amount of the putative transcription factor that binds to both P1 and P1\u2032 promoter regions is present in the cytosol of vancomycin-induced cells. Neither the SigB sigma factor nor the quorum-sensing\n            <jats:italic>agr<\/jats:italic>\n            locus was required for growth phase-variable\n            <jats:italic>pbpB<\/jats:italic>\n            expression or transcriptional induction of\n            <jats:italic>pbpB<\/jats:italic>\n            by vancomycin or oxacillin. Also, MecI, MecR1, BlaI, and BlaR1, regulatory proteins that mediate \u03b2-lactam-inducible expression of\n            <jats:italic>mecA<\/jats:italic>\n            and \u03b2-lactamase, were not required for antibiotic induction of\n            <jats:italic>pbpB<\/jats:italic>\n            transcription. These data support the idea that\n            <jats:italic>pbpB<\/jats:italic>\n            expression is modulated by a\n            <jats:italic>trans<\/jats:italic>\n            -acting factor in response to the presence of the cell wall-active antibiotics vancomycin and oxacillin.\n          <\/jats:p>","DOI":"10.1128\/aac.47.3.1028-1036.2003","type":"journal-article","created":{"date-parts":[[2003,2,25]],"date-time":"2003-02-25T18:22:21Z","timestamp":1046197341000},"page":"1028-1036","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":42,"title":["Transcriptional Induction of the Penicillin-Binding Protein 2 Gene in\n            <i>Staphylococcus aureus<\/i>\n            by Cell Wall-Active Antibiotics Oxacillin and Vancomycin"],"prefix":"10.1128","volume":"47","author":[{"given":"Susan","family":"Boyle-Vavra","sequence":"first","affiliation":[{"name":"Department of Pediatrics"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shaohui","family":"Yin","sequence":"additional","affiliation":[{"name":"Department of Pediatrics"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mamatha","family":"Challapalli","sequence":"additional","affiliation":[{"name":"Department of Pediatrics"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert S.","family":"Daum","sequence":"additional","affiliation":[{"name":"Department of Pediatrics"},{"name":"Committee on Microbiology"},{"name":"Committee on Molecular Medicine, The University of Chicago, Chicago, Illinois 60637"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1007\/s000180050023"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1007\/BF02013308"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.45.6.1714-1720.2001"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1574-6968.2001.tb09449.x"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1093\/jac\/48.5.617"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1128\/jb.179.21.6756-6763.1997"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.45.1.280-287.2001"},{"key":"e_1_3_2_9_2","first-page":"565","volume":"51","year":"2002","unstructured":"Centers for Disease Control and Prevention. 2002. 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