Transcription activator involved in multidrug resistance, oxidative stress response, and redox homeostasis. Preferentially binds to promoters with the core binding site 5'-TTA[CG]TAA-3'. Involved in the oxidative stress response in via multiple pathways, including the cellular antioxidant defense system, carbohydrate metabolism and energy metabolism, protein degradation, ATP-dependent RNA helicase, and resistance pathways. The ability of the major systemic fungal pathogen of humans to sense and respond to reactive oxygen species, such as H(2)O(2) generated by the host immune system, is required for survival in the host and therefore virulence. Regulates the transcription of COR33, GLR1, GTO1, GTT1, GTT1, TRR1, TRX1, SOD1, CAT1, and the transcription regulator TSA1. Participates in the apoptosis by regulating the expression of the glutathione reductase gene and glutathione content. Also plays a role in the peroxide-mediated induction of MDR1 and other drug response genes such as PDR16, MDR1, FLU1, YCF1, and FCR1. Regulates trehalose accumulation which is important for the oxidative stress tolerance. Recruits ADA2 to its target promoters. Activity of CAP1 is controlled through oxidation of specific cysteine residues resulting in the alteration of its subcellular location. Oxidative stress induces nuclear accumulation and as a result CAP1 transcriptional activity. Nuclear export is restored when disulfide bonds are reduced by thioredoxin, whose expression is controlled by CAP1, providing a mechanism for negative autoregulation. Interacts with YBP1. Oxidized CAP1 is found predominantly in the nucleus, while reduced CAP1 is continuously exported to the cytoplasm. Caspofungin treatment also induces nuclear translocation. Induced by oxidative stress and during contact with neutrophils. Expression is also up-regulated by the thioredoxin TRX1 and by treatment with Chinese herbal medicine baicalein. Contains two cysteine rich domains (CRD), referred to as the N- and C-terminal CRD's, n-CRD (Cys-254 and Cys-261) and c-CRD (Cys-446, Cys-468 and Cys-477), respectively. A nuclear export signal is embedded in the c-CRD, with which the nuclear export protein CRM1/exportin 1 interacts only in the absence of disulfide bonds (or otherwise oxidized cysteines) within the c-CRD or between the c-CRD and the n-CRD. Upon oxidative stress, is oxidated by the peroxidase GPX3 and stabilized by YBP1 (PubMed:20679492, PubMed:23706023). Oxidative stress induces conformational changes through oxidation of cysteine residues, masking the nuclear export signal, thus abolishing nuclear export by CRM1/exportin 1 (By similarity). Phosphorylated in response to H(2)O(2). Causes hypersensitivity to cadmium, 4-nitroquinoline N-oxide, 1,10-phenanthroline, and hydrogen peroxide. Abolishes the peroxide-mediated induction of COR33, TSA1, and many other genes involved in oxidative stress response. Inhibits trehalose accumulation upon exposure to oxidative stress. Shows significantly reduced viability when exposed to whole blood or polymorphonuclear cells, as well as to the Chinese herbal medicine baicalein. Leads also to decreased virulence in a Caenorhabditis elegans model. Increases apoptosis upon apoptotic stimulation. Belongs to the bZIP family. YAP subfamily.