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Nucleotide excision repair is a DNA repair mechanism. [2] DNA damage occurs constantly because of chemicals (e.g. intercalating agents ), radiation and other mutagens . Three excision repair pathways exist to repair single stranded DNA damage: Nucleotide excision repair (NER), base excision repair (BER), and DNA mismatch repair (MMR).
DNA repair is a collection of processes by which a cell identifies and corrects damage to the DNA molecules that encode its genome. [1] In human cells, both normal metabolic activities and environmental factors such as radiation can cause DNA damage, resulting in tens of thousands of individual molecular lesions per cell per day. [2]
A DNA repair-deficiency disorder is a medical condition due to reduced functionality of DNA repair. DNA repair defects can cause an accelerated aging disease or an increased risk of cancer , or sometimes both.
Base excision repair (BER) is a cellular mechanism, studied in the fields of biochemistry and genetics, that repairs damaged DNA throughout the cell cycle. It is responsible primarily for removing small, non-helix-distorting base lesions from the genome.
The DNA repair mechanism involving photolyases is called photoreactivation. They mainly convert pyrimidine dimers into a normal pair of pyrimidine bases. Photo reactivation, the first DNA repair mechanism to be discovered, was described initially by Albert Kelner in 1949 [ 3 ] and independently by Renato Dulbecco also in 1949.
Nucleotide excision repair (NER) is a major pathway for repairing a variety of bulky DNA damages including those introduced by UV irradiation. The XPA protein appears to play a key role in NER at sites of damage as a scaffold for other repair proteins in order to ensure that the damages are appropriately excised. [5]