Gene Ontology annotation through association of InterPro records with 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 UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Electronic Gene Ontology annotations created by ARBA machine learning models
Role of TFP1 in vacuolar acidification, oxidative stress and filamentous development in Candida albicans.
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Tfp1 is a putative C. albicans V-ATPase subunit that is essential for vacuolar acidification and endocytic trafficking.
"In this study, we identified C. albicans Tfp1 as a putative subunit of V-ATPase, and explored its importance in multiple cellular processes. Our results revealed that Tfp1 played an essential role in vacuolar acidification and endocytic trafficking."
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Loss of TFP1 perturbs oxidative-stress physiology and reduces Cap1 expression after hydrogen peroxide treatment.
"Western blotting analysis showed that deletion of TFP1 significantly reduced the expression of Cap1 under H2O2 treatment, which contributes to the regulation of genes involved in the oxidative stress response."
Tfp1 is required for ion homeostasis, fluconazole resistance and N-Acetylglucosamine utilization in Candida albicans.
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TFP1 deletion disrupts iron, copper, and calcium homeostasis and alters fluconazole and N-acetylglucosamine physiology.
"In this study, we demonstrated the essential roles of V-ATPase through Tfp1, a putative V-ATPase subunit. Deletion of TFP1 led to generation of an iron starvation signal and reduced total iron content, which was associated with mislocalization of Fet34p that was finally due to disorders in copper homeostasis."
Effects of Disruption of PMC1 in the tfp1∆/∆ Mutant on Calcium Homeostasis, Oxidative and Osmotic Stress Resistance in Candida albicans.
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Further deletion of the vacuolar calcium pump PMC1 in a tfp1 mutant exacerbates calcium-homeostasis and stress phenotypes.
"In this study, we found that further deletion of PMC1, a vacuolar calcium pump, in tfp1∆/∆ mutant led to more severe dysregulation of calcium homeostasis."