{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,29]],"date-time":"2026-10-29T07:41:29Z","timestamp":1793259689134,"version":"4.5.0"},"reference-count":34,"publisher":"American Society for Microbiology","issue":"8","license":[{"start":{"date-parts":[[2004,8,1]],"date-time":"2004-08-01T00:00:00Z","timestamp":1091318400000},"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":[[2004,8]]},"abstract":"ABSTRACT<\/jats:title>\n \n Azole resistance in\n Candida albicans<\/jats:italic>\n can be due to upregulation of multidrug transporters belonging to ABC (ATP-binding cassette) transporters (\n CDR1<\/jats:italic>\n and\n CDR2<\/jats:italic>\n ) or major facilitators (\n CaMDR1<\/jats:italic>\n ). Upregulation of these genes can also be achieved by exposure to fluphenazine, resulting in specific upregulation of\n CDR1<\/jats:italic>\n and\n CDR2<\/jats:italic>\n and by exposure to benomyl, resulting in specific\n CaMDR1<\/jats:italic>\n upregulation. In this study, these two different states of gene upregulation were used to determine coregulated genes that often share similar functions or similar regulatory regions. The transcript profiles of a laboratory strain exposed to these drugs were therefore determined and compared with those of two matched pairs of azole-susceptible and -resistant strains expressing\n CDR1<\/jats:italic>\n and\n CDR2<\/jats:italic>\n (CDR strains) or\n CaMDR1<\/jats:italic>\n (MDR isolates). The results obtained revealed that, among 42 commonly regulated genes (8.6% of all regulated genes) between fluphenazine-exposed cells and CDR isolates, the most upregulated were\n CDR1<\/jats:italic>\n and\n CDR2<\/jats:italic>\n as expected, but also\n IFU5<\/jats:italic>\n ,\n RTA3<\/jats:italic>\n (which encodes putative membrane proteins),\n HSP12<\/jats:italic>\n (which encodes heat shock protein), and\n IPF4065<\/jats:italic>\n (which is potentially involved in stress response). Interestingly, all but\n HSP12<\/jats:italic>\n and\n IPF4065<\/jats:italic>\n contain a putative\n cis<\/jats:italic>\n -acting drug responsive element in their promoters. Among the 57 genes (11.5% of all regulated genes) commonly regulated between benomyl-exposed cells and MDR isolates, the most upregulated were\n CaMDR1<\/jats:italic>\n as expected but also genes with oxido-reductive functions such as\n IFD<\/jats:italic>\n genes,\n IPF5987<\/jats:italic>\n ,\n GRP2<\/jats:italic>\n (all belonging to the aldo-keto reductase family),\n IPF7817<\/jats:italic>\n [NAD(P)H oxido-reductase], and\n IPF17186<\/jats:italic>\n . Taken together, these results show that in vitro drug-induced gene expression only partially mimics expression profiles observed in azole-resistant clinical strains. Upregulated genes in both drug-exposed conditions and clinical strains are drug resistance genes but also genes that could be activated under cell damage conditions.\n <\/jats:p>","DOI":"10.1128\/aac.48.8.3064-3079.2004","type":"journal-article","created":{"date-parts":[[2004,7,23]],"date-time":"2004-07-23T14:45:20Z","timestamp":1090593920000},"page":"3064-3079","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":157,"title":["Comparison of Gene Expression Profiles of\n Candida albicans<\/i>\n Azole-Resistant Clinical Isolates and Laboratory Strains Exposed to Drugs Inducing Multidrug Transporters"],"prefix":"10.1128","volume":"48","author":[{"given":"Mahir","family":"Karababa","sequence":"first","affiliation":[{"name":"Institut de Microbiologie, Centre Hospitalier Universitaire Vaudois, 1011 Lausanne, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alix T.","family":"Coste","sequence":"additional","affiliation":[{"name":"Institut de Microbiologie, Centre Hospitalier Universitaire Vaudois, 1011 Lausanne, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Be\u0301ne\u0301dicte","family":"Rognon","sequence":"additional","affiliation":[{"name":"Institut de Microbiologie, Centre Hospitalier Universitaire Vaudois, 1011 Lausanne, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jacques","family":"Bille","sequence":"additional","affiliation":[{"name":"Institut de Microbiologie, Centre Hospitalier Universitaire Vaudois, 1011 Lausanne, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dominique","family":"Sanglard","sequence":"additional","affiliation":[{"name":"Institut de Microbiologie, Centre Hospitalier Universitaire Vaudois, 1011 Lausanne, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M306291200"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/JB.181.3.700-708.1999"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.44.5.1255-1265.2000"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1128\/jcm.34.5.1235-1248.1996"},{"key":"e_1_3_2_6_2","unstructured":"Calabrese D. 2002. 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