XP (Xeroderma pigmentosum) is an autosomal recessive human disease characterized by hypersensitivity to sunlight and a high incidence of skin cancer on sunexposed skin (1). Cells from XP patients are hypersensitive to killing by UV irradiation beause of a defect in nucleotide excision repair (NER). XP is classified into seven complementation groups (A~G) and a variant form (1). XPA shows the most severe symptoms. Products encoded by the XP genes function in repairing UV-induced cyclobutane pyrimidine dimmer and (6-4) photoproducts as well as chemically induced variety of DNA lesions (1). XPA protein consists of 273 amino acids and forms a complexe with many proteins such as RPA, ERCC1, TFIIH、XAB1, and XAB2, which play a role in early step of NER. The hybrydoma 5F12 was constructed by Pro. K. Tanaka’ group who first cloned the XPA gene (2, 3) .
1) Western blotting (0.1~1 ug/ml)
3) Inhibition of in vitro excision repair reaction.
4) Inhibition of XPA interaction with ERCC1 and TFIIH
Detection of XPA protein in crude extract of HeLa cell by western blotting, using the monoclonal antibody 5F12.
To be used for research only. DO NOT use for human gene therapy or clinical diagnosis.