Involved in DNA excision repair. Initiates repair by binding to damaged sites with various affinities, depending on the photoproduct and the transcriptional state of the region. Required for UV-induced CHEK1 phosphorylation and the recruitment of CEP164 to cyclobutane pyrimidine dimmers (CPD), sites of DNA damage after UV irradiation (By similarity). Interacts with GPN1. Interacts with RPA1 and RPA2; the interaction is direct and associates XPA with the RPA complex. Interacts (via N-terminus) with CEP164 upon UV irradiation. Interacts with HERC2 (By similarity). Exhibits a circadian pattern with zenith at around 5 pm and nadir at around 5 am in liver but not in testis, this oscillation is dependent on the circadian clock and on HERC2 regulation. Ubiquitinated by HERC2 leading to degradation by the proteasome. Deficient mice cannot repair UV-induced DNA damage and easily develop skin cancers by UV irradiation. They develop stronger longer-lasting acute inflammation, they show a more severe UV-induced damage of keratinocytes and Langerhans cells as well as the enhancement of local and systemic immunosuppression. PGE2 and COX2 expression is greatly increased after UVB irradiation, this causes the enhancement of inflammation and immunosuppression. Natural killer cell activity is also significantly decreased. Plays an essential role in the repair of cisplatin induced damage by nucleotide excision repair. Cisplatin is one of the most commnly used anticancer drugs. Belongs to the XPA family.