Nucleotide excision repair is a DNA repair mechanism that repairs DNA damaged by UV radiation. This type of damage produces bulky distortions in the shape of DNA double helix due to the addition of DNA adducts, mostly thymine dimers and 6,4-photoproducts.
Recognition of distortions leads to the removal of a short single-stranded DNA segment that includes the lesion, creating a single-strand gap in the DNA. That is subsequently filled in by DNA polymerase, which uses the undamaged strand as a template. NER can be divided into two subpathways (blobal genomic NER and transcription coupled NER) that differ only in their recognition of helix-distorting DNA damage. Nucleotide excision repair has more complexity in eukaryotes.
Nucleotide excision repair (NER) is a particularly important DNA repair mechanism as evidenced by the severe human diseases that result from in-born genetic mutations of NER proteins including xeroderma pigmentosum and Cockayne syndrome.
This pathway was adapted from [KEGG](https://www.genome.jp/dbget-bin/www_bget?pathway+hsa03420), [REPAIRtoire](http://repairtoire.genesilico.pl/Pathway/2/), and [Wikipedia](https://en.wikipedia.org/wiki/Nucleotide_excision_repair). The pathway layout is based on KEGG.
This pathway describes the process of Nucleotide Excision Repair (NER) in Xeroderma Pigmentosum (XP).