MS-based quantitative proteomic analysis of UVB irradiation in XPC-deficient keratinocytes

Xeroderma Pigmentosum C (XPC) is a DNA damage recognition protein central to the global genome nucleotide excision repair (GG-NER) pathway, where it acts as a primary sensor of UV-induced DNA lesions. Loss-of-function mutations in the XPC gene lead to a photosensitive phenotype, with marked accumulation of unrepaired DNA damage and a dramatically elevated risk (10,000-fold) of skin cancer. This work aims at understanding the molecular signaling mechanisms associated with XP-C using genetically engineered human XPC knockout (KO) keratinocytes, the predominant cell type affected by UV radiation. We performed a mass spectrometry (MS)-based quantitative proteomic analysis, comparing XPC-wild-type and XPC-KO keratinocytes exposed or not to UVB for 24 hours.