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dc.contributor.author Antonella en_US
dc.contributor.author Romano en_US
dc.contributor.author Mario en_US
dc.contributor.author Mario en_US
dc.contributor.author Steven L. en_US
dc.date.accessioned 2009-12-15T14:43:07Z
dc.date.available 2009-12-15T14:43:07Z
dc.date.issued 2002 en_US
dc.identifier http://dx.doi.org/10.1016/S1471-4914(02)02280-3 en_US
dc.identifier.citation Lupetti , A , Danesi , R , Campa , M , Del Tacca , M & Kelly , S L 2002 , ' Molecular basis of resistance to azole antifungals ' Trends in Molecular Medicine , vol 8 , no. 2 , pp. 76-81 . , 10.1016/S1471-4914(02)02280-3 en_US
dc.identifier.other PURE: 134338 en_US
dc.identifier.other dspace: 2160/3827 en_US
dc.identifier.uri http://hdl.handle.net/2160/3827
dc.description.abstract The increased incidence of invasive mycoses and the emerging problem of antifungal drug resistance has prompted investigations of the underlying molecular mechanisms, particularly for the azole compounds central to current therapy. The target site for the azoles is the ERG11 gene product, the cytochrome P450 lanosterol 14α-demethylase, which is part of the ergosterol biosynthetic pathway. The resulting ergosterol depletion renders fungal cells vulnerable to further membrane damage. Development of azole resistance in fungi may occur through increased levels of the cellular target, upregulation of genes controlling drug efflux, alterations in sterol synthesis and decreased affinity of azoles for the cellular target. Here, we review the adaptative changes in fungi, in particular Candida albicans, in response to inhibitors of ergosterol biosynthesis. The molecular mechanisms of azole resistance might help in devising more effective antifungal therapies. en_US
dc.format.extent 6 en_US
dc.relation.ispartof Trends in Molecular Medicine en_US
dc.title Molecular basis of resistance to azole antifungals en_US
dc.contributor.pbl Aberystwyth University en_US
dc.contributor.pbl Institute of Biological, Environmental and Rural Sciences en_US


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