Use of the ND evidence code for Gene Ontology (GO) terms
Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniPathway vocabulary mapping
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
UniProtKB record for C. albicans ERG2
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C. albicans ERG2 is annotated as a sterol C-8 isomerase that catalyzes the fecosterol-to-episterol reaction in the late ergosterol biosynthetic pathway.
"Reaction=fecosterol = episterol"
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UniProt places C. albicans ERG2 at the endoplasmic reticulum membrane.
"SUBCELLULAR LOCATION: Endoplasmic reticulum membrane"
Membrane sphingolipid-ergosterol interactions are important determinants of multidrug resistance in Candida albicans.
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The C. albicans erg2 mutant shows altered susceptibility to several xenobiotics, consistent with drug-response phenotypes downstream of perturbed ergosterol biosynthesis.
"erg2 and erg16 mutant cells of C. albicans became hypersensitive"
Ergosterol gene expression in wild-type and ergosterol-deficient mutants of Candida albicans.
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Pierson et al. generated viable C. albicans ergosterol-biosynthetic mutants, including an erg2 mutant.
"developed a panel of five viable ergosterol biosynthetic mutants (erg2, erg3,"
Genome-wide fitness test and mechanism-of-action studies of inhibitory compounds in Candida albicans.
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The main CaFT article profiled known and novel inhibitory compounds in a C. albicans heterozygous deletion pool; the ERG2-specific hit for an ergosterol inhibitor is in supplemental data not present in the local cache.
"The profiles of additional inhibitors of ergosterol biosynthesis, including terbinafine, lovastatin, and dyclonine, are described in Text S1"
Fitness trade-offs restrict the evolution of resistance to amphotericin B.
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Laboratory C. albicans ERG2 loss was sufficient to produce amphotericin B resistance, reinforcing that ERG2-dependent sterol chemistry shapes antifungal susceptibility.
"loss of ERG2 or the combined loss of ERG3 and ERG11 function is sufficient to confer resistance to AmB"
ERG2 and ERG24 are required for normal vacuolar physiology as well as Candida albicans pathogenicity in a murine model of disseminated but not vaginal candidiasis.
The Adr1 transcription factor directs regulation of the ergosterol pathway and azole resistance in Candida albicans.
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Candida Adr1 acts as a transcriptional regulator of the ergosterol pathway, adding recent regulatory context around ERG2 expression.
"We have identified the TF Adr1 as a key regulator of sterol biosynthesis in the fungal pathogen C. albicans"