Nucleotide excision repair (NER) is an important DNA repair mechanism by which the cell repairs DNA damage occurring to bases. Base damage can be caused by a variety of sources including chemicals and UV light. NER is the mechanism by which the cell can prevent unwanted mutations by removing the majority of UV-induced DNA damage (mostly in the form of thymine dimmers and 6-4-photoproducts). The importance of this repair mechanism is evidenced by the severe human diseases that result from in-born genetic mutations of NER proteins, including Xeroderma pigmentosum and Cockayne's syndrome. NER recognizes bulky distortions in the shape of the DNA double helix. Recognition of these distortions leads to the removal of a short single-stranded DNA segment that includes the lesion, creating a single-stranded gap in the DNA. This gap is subsequently filed in by DNA polymerase, using the undamaged strand as a template.
All Nucleotide-Exicision Repair Antibodies, Lysates, Proteins, and RNAi