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dc.contributor.authorChen, CGen_US
dc.contributor.authorYang, YLen_US
dc.contributor.authorShih, HIen_US
dc.contributor.authorSu, CLen_US
dc.contributor.authorLo, HJen_US
dc.date.accessioned2014-12-08T15:37:13Z-
dc.date.available2014-12-08T15:37:13Z-
dc.date.issued2004-12-01en_US
dc.identifier.issn0066-4804en_US
dc.identifier.urihttp://dx.doi.org/10.1128/AAC.48.12.4505-4512.2004en_US
dc.identifier.urihttp://hdl.handle.net/11536/25574-
dc.description.abstractOverexpression of CDR1, an efflux pump, is one of the major mechanisms contributing to drug resistance in Candida albicans. CDR1 p-lacZ was constructed and transformed into a Saccharomyces cerevisiae strain so that the lacZ gene could be used as the reporter to monitor the activity of the CDR1 promoter. Overexpression of CaNDT80, the C albicans homolog of S. cerevisiae NDT80, increases the beta-galactosidase activity of the CDR1 p-lacZ construct in S. cerevisiae. Furthermore, mutations in CaNDT80 abolish the induction of CDR1 expression by antifungal agents in C albicans. Consistently, the Candt80/Candt80 mutant is also more susceptible to antifungal drugs than the wild-type strain. Thus, the gene for CaNdt80 may be the first gene among the regulatory factors involved in drug resistance in C. albicans whose function has been identified.en_US
dc.language.isoen_USen_US
dc.titleCaNdt80 is involved in drug resistance in Candida albicans by regulating CDR1en_US
dc.typeArticleen_US
dc.identifier.doi10.1128/AAC.48.12.4505-4512.2004en_US
dc.identifier.journalANTIMICROBIAL AGENTS AND CHEMOTHERAPYen_US
dc.citation.volume48en_US
dc.citation.issue12en_US
dc.citation.spage4505en_US
dc.citation.epage4512en_US
dc.contributor.department生物科技學系zh_TW
dc.contributor.departmentDepartment of Biological Science and Technologyen_US
dc.identifier.wosnumberWOS:000225474500002-
dc.citation.woscount38-
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