Transcription factor involved in the regulation of ergosterol biosynthetic genes such as ERG2 and ERG11 through direct binding to sterol response elements (SREs) in the promoters. Binds also to its own promoter on 2 cis-acting elements to promote autoregulation. Regulates sterol uptake across the plasma membrane. Acts as a major regulator of ascorbic acid-induced response. Plays a role in the triggering of pyroptosis, an inflammasome-mediated programmed cell death pathway in macrophages, allowing macrophages escaping. Expression is up-regulated by ergosterol depletion, by azoles, and in anaerobic conditions. Transcript is repressed during co-incubated with macrophages, a condition that induces filamentous growth. Promotes positive auto-regulation through binding to its own promoter. Shows increased susceptibility to the azole drugs ketoconazole, itraconazole, and fluconazole; drugs that act on ergosterol biosynthesis such as terbinafine, fenpropimorph, and lovastatin; as well as malachite green. Leads to lower ergosterol levels. Decreases pyroptosis but has little effect on filamentation in the macrophage. Gain-of-function mutations in UPC2 are more prevalent among clinical isolates than previously thought and make a significant contribution to azole antifungal resistance.