核苷酸切除修复(NER)是一种主要的修复系统，用于清除各种DNA损伤，包括紫外线诱导的环丁烷嘧啶二聚体和(6-4)光产物以及化学诱导的大块碱基加合物。NER系统缺陷导致色素性干皮病(XP)，这是一种常染色体隐性疾病，其特征是易患皮肤癌，在某些情况下神经系统异常。人类NER的早期过程，从损伤识别到双切口(去除含损伤寡核苷酸)，是由六个核心NER因子XPC-RAD23B、TFIIH、XPA、RPA、XPF-ERCC1和XPG完成的。
XPG是一种与ERCC1-XPF极性相反的结构特异性内切酶，它在DNA链上形成一个缺口，使5’到3’方向上的单链DNA转变为双链DNA。在NER过程中，XPG在双切口步骤中负责3’切口。
Anti DNA Repair Protein Complementing XP-G Cells (XPG/ERCC5) mAb (Clone G-26),CAC-KUP-TM-M03
Application: WB
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.
XPG is a structure-specific endonuclease with an opposite polarity to ERCC1-XPF and makes a nick on the DNA strand which makes the transition from single-stranded to duplex DNA in the 5′ to 3′ direction. In the NER process, XPG is responsible for 3′-incision at a dual incision step.