Anti DNA Repair Protein Complementing XP-A Cells (XPA) mAb (Clone 5F12)

Nucleotide excision repair (NER) is a major repair system for removing a variety of DNA lesions including UV-induced cyclobutane pyrimidine dimers and (6-4) photoproducts as well as chemically-induced bulky base adducts. Defects in the NER system give rise to xeroderma pigmentosum (XP), an autosomal recessive disease characterized by a predisposition to skin cancer and in some cases neurological abnormalities. The early process of human NER, from damage recognition to dual incision (removal of damage-containing oligonucleotides), is accomplished by six core NER factors, XPC-RAD23B, TFIIH, XPA, RPA, XPF-ERCC1 and XPG.

XP (Xeroderma pigmentosum) is an autosomal recessive human disease characterized by hypersensitivity to sunlight and a high incidence of skin cancer on sun-exposed skin (1). Cells from XP patients are hypersensitive to killing by UV irradiation because 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 complex with many proteins such as RPA, ERCC1, TFIIH, XAB1, and XAB2, which play roles in early steps of NER.

The hybridoma 5F12 was constructed by Prof. K. Tanaka’s group who first cloned the XPA gene (2, 3).

References:
1) Friedberg E C et. al., DNA Repair and Mutagenesis 2nd ed., ASM Press (2006).
2) Saijo M et al “Inhibition of nucleotide excision repair by anti-XPA monoclonal antibodies which interefere with
binding to RPA, ERCC1, and TFIIH” Biochem Biophys Res Comm 321:815-822 (2004). PMID: 15358100
3) Tanaka K et al “Analysis of a human DNA excision repair gene involved in group A xeroderma pigmentosum
and containing a zinc-finger domain” Nature 348:73 -76 (1990). PMID: 2234061