Description
Clonality: Monoclonal
Host: Mouse
Purification: Ammonium Sulfate
Reactivity: Human
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.
XPA has an ability to bind to DNA with some preference to damaged DNA and interacts with most of other NER factors. XPA appears to be involved in a proper assembly of preincision complex and verification of damaged DNA strand.
References:
Nagao A, Zhao X, Takegami T, et al., Multiple shRNA expressions in a single plasmid vector improve RNAi against the XPA gene. Biochem. Biophys. Res. Commun. 370, 301-305, 2008.
