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. Plays also 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.
