Anti-XPG/ERCC5 Antibody Picoband®

This gene encodes a single-strand specific DNA endonuclease that makes the 3' incision in DNA excision repair following UV-induced damage. The protein may also function in other cellular processes, including RNA polymerase II transcription, and transcription-coupled DNA repair. Mutations in this gene cause xeroderma pigmentosum complementation group G (XP-G), which is also referred to as xeroderma pigmentosum VII (XP7), a skin disorder characterized by hypersensitivity to UV light and increased susceptibility for skin cancer development following UV exposure. Some patients also develop Cockayne syndrome, which is characterized by severe growth defects, cognitive disability, and cachexia. Read-through transcription exists between this gene and the neighboring upstream BIVM (basic, immunoglobulin-like variable motif containing) gene.

ERCC5; ERCM2; XPG; XPGC; DNA repair protein complementing XP-G cells; EC 3.1.-.-; DNA excision repair protein ERCC-5; Xeroderma pigmentosum group G-complementing protein

E.coli-derived human XPG/ERCC5 recombinant protein (Position: K115-R964) . Human XPG/ERCC5 shares 66.6% amino acid (aa) sequence identity with mouse XPG/ERCC5.

1. Arlett, C. F., Harcourt, S. A., Lehman, A. R., Stevens, S., Ferguson-Smith, M. A., Morley, W. N. Studies on a new case of xeroderma pigmentosum (XP3BR) from complementation group G with cellular sensitivity to ionizing radiation. Carcinogenesis 1: 745-751, 1980. 2. Cheesbrough, M. J. Xeroderma pigmentosum--a unique variant with neurological involvement. Brit. J. Derm. 99 (Suppl. 16) : 61 only, 1978. 3. Cleaver, J. E., Thompson, L. H., Richardson, A. S., States, J. C. A summary of mutations in the UV-sensitive disorders: xeroderma pigmentosum, Cockayne syndrome, and trichothiodystrophy. Hum. Mutat. 14: 9-22, 1999.

At -20°C for one year from date of receipt. After reconstitution, at 4°C for one month. It can also be aliquotted and stored frozen at -20°C for six months. Avoid repeated freezing and thawing.