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dc.contributor.authorYang, YLen_US
dc.contributor.authorChen, HFen_US
dc.contributor.authorKuo, TJen_US
dc.contributor.authorLin, CYen_US
dc.date.accessioned2014-12-08T15:16:44Z-
dc.date.available2014-12-08T15:16:44Z-
dc.date.issued2006-05-01en_US
dc.identifier.issn1021-7770en_US
dc.identifier.urihttp://dx.doi.org/10.1007/s11373-005-9054-6en_US
dc.identifier.urihttp://hdl.handle.net/11536/12325-
dc.description.abstractEnolase ( 2- phospho- (D)- glycerate hydrolase) is an enzymatic component of the glycolytic pathway and is conserved through evolution. The TR- CaENO1/ Caeno1 stain, of which the expression of CaENO1 is under control of the tetracycline- regulatable ( TR) expression system, is utilized for elucidating the functions of CaENO1 in Candida albicans. As expected, there was no detectable CaENO1 mRNA when the TR- CaENO1/ Caeno1 cells grew on media containing doxycycline repressing the expression of TR- CaENO1. The TR- CaENO1/ Caeno1 cells were arrested in media containing doxycycline in the presence of glucose but not in non- fermentable carbon sources, such as glycerol. Furthermore, the TR- CaENO1/ Caeno1 cells were also arrested in media containing 4% serum. In this study, we have showed that CaENO1 is required for the cell growth of C. albicans in the presence of glucose. Our findings may help us to design new and more effective antifungal agents for preventing and treating bloodstream fungal infections by blocking the function( s) of enolases.en_US
dc.language.isoen_USen_US
dc.subjectCandida albicansen_US
dc.subjectcell growthen_US
dc.subjectenolaseen_US
dc.subjectglucoseen_US
dc.subjectinhibitionen_US
dc.titleMutations on CaENO1 in Candida albicans inhibit cell growth in the presence of glucoseen_US
dc.typeArticleen_US
dc.identifier.doi10.1007/s11373-005-9054-6en_US
dc.identifier.journalJOURNAL OF BIOMEDICAL SCIENCEen_US
dc.citation.volume13en_US
dc.citation.issue3en_US
dc.citation.spage313en_US
dc.citation.epage321en_US
dc.contributor.department生物科技學系zh_TW
dc.contributor.departmentDepartment of Biological Science and Technologyen_US
dc.identifier.wosnumberWOS:000237502100004-
dc.citation.woscount4-
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