Anti DNA Repair Protein Complementing XP-G Cells (XPG/ERCC5) mAb (Clone G-26)

Antibodies/Primary Antibodies/DNA Damage & Repair; Antibodies/DNA Damage & Repair/Primary Antibodies; Research Area/Cell Biology/DNA Damage & Repair/Primary Antibodies; Research Area/Cell Biology/UV Induced DNA Damage/Primary Antibodies; Research Area/Cell Biology/Gene Expression & Transcription/Primary Antibodies; Research Area/Disease/Xeroderma Pigmentosum/Primary Antibodies; Research Area/Disease/COFS/Primary Antibodies; Research Area/Disease/Deafness/Primary Antibodies; Research Area/Cell Biology/Homologous Recombination/Primary Antibodies; Research Area/Cell Biology/Apoptosis/Primary Antibodies

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.
References:
Oyama M, Wakasugi M, Hama T, et al., Human NTH1 physically interacts with p53 and proliferating cell nuclear antigen. Biochem. Biophys. Res. Commun. 321, 183-191 (2004).

Monoclonal