Mediates oxidative stress response. Involved in both the oxidative and cadmium response pathways.
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Transcription activator involved in oxidative stress response and redox homeostasis. Regulates the transcription of genes encoding antioxidant enzymes and components of the cellular thiol-reducing pathways, including the thioredoxin system (TRX2, TRR1), the glutaredoxin system (GSH1, GLR1), superoxide dismutase (SOD1, SOD2), glutathione peroxidase (GPX2), and thiol-specific peroxidases (TSA1, AHP1). The induction of some of these genes requires the cooperative action of both, YAP1 and SKN7. YAP1 preferentially binds to promoters with the core binding site 5'-TTA[CG]TAA-3'. Activity of YAP1 is controlled through oxidation of specific cysteine residues resulting in the alteration of its subcellular location. Oxidative stress (as well as carbon stress, but not increased temperature, acidic pH, or ionic stress) induces nuclear accumulation and as a result YAP1 transcriptional activity. Nuclear export is restored when disulfide bonds are reduced by thioredoxin (TRX2), whose expression is controlled by YAP1, providing a mechanism for negative autoregulation. When overexpressed, YAP1 confers pleiotropic drug-resistance and increases cellular tolerance to cadmium, iron chelators and zinc.
Transcription activator involved in the regulation of genes expressed in response to environmental changes and metabolic requirements. According to genome-wide promoter binding and gene expression studies it regulates, among others, genes involved in ribosome biogenesis, and protein synthesis. It may also be involved in pleiotropic drug resistance. When overexpressed it confers increased resistance to cisplatin, the DNA-alkylating agents methylmethanosulfonate, and mitomycin C, the antimalarial drugs quinidine, mefloquine, and chloroquine, and increases cellular tolerance to sodium and lithium. Preferentially binds 5'-TTACTAA-3'.
Transcription activator of genes coding for transmembrane transporters (ACR2 and ACR3) involved in resistance to arsenic oxide. Its transcription activity is greatly induced by arsenite in a dose-dependent manner.
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