Year: 2020
Type: article
Abstract: Azole drugs act by blocking the biosynthesis of ergosterol, the sterol component of the fungal plasma membrane.Resistance to azole drugs appears frequently in fungi and can be typically acquired by changes in the coding sequence of the gene producing lanosterol 14α-demethylase, the azole target enzyme, or changes in the expression of this gene that is designated ERG11 [1].A second route of resistance involves increased expression of loci encoding ATPbinding cassette (ABC) transporters, which are thought to efflux drugs and prevent toxic intracellular concentrations from being achieved [2].These 2 resistance mechanisms have generally been considered to represent independent, unlinked modes of lowering azole susceptibility.Recent work in several different fungi support a different viewpoint: that these resistance modalities actually illuminate a physiological tie between the biosynthesis of ergosterol and expression of ABC transporter proteins.
Source: PLoS Pathogens
Author: W. Scott Moye-Rowley
Institution: University of Iowa
Language: English
Subfield: Infectious Diseases
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $2,500
Awards: Genetic analysis of pleiotropic drug resistance, Genetic analysis of pleiotropic drug resistance, Identification of virulence determinants under the transcriptional control of AtrR in Aspergillus fumigatus, Elevated gene transcription of the cyp51A gene is essential for azole drug resistance in Aspergillus fumigatus
OpenAlex ID: W3083609144