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These findings thus indicate that the repair of thymine dimers in wild-type yeast is highly efficient. [citation needed] Nucleotide excision repair, sometimes termed "dark reactivation", is a more general mechanism for repair of lesions and is the most common form of DNA repair for pyrimidine dimers in humans. This process works by using ...
Nucleotide excision repair (NER) is a particularly important excision mechanism that removes DNA damage induced by ultraviolet light (UV). UV DNA damage results in bulky DNA adducts — these adducts are mostly thymine dimers and 6,4-photoproducts. Recognition of the damage leads to removal of a short single-stranded DNA segment that contains ...
Photolyases have a high affinity for these lesions and reversibly bind and convert them back to the original bases. The photolyase-catalyzed DNA repair process by which cyclobutane pyrimidine dimers are resolved has been studied by time-resolved crystallography and computational analysis to allow atomic visualization of the process. [8]
Ultraviolet (UV) light induces the formation of DNA damages including pyrimidine dimers (such as thymine dimers) and 6,4 photoproducts. These types of "bulky" damages are repaired by nucleotide excision repair. [citation needed]
Review articles, [116] and broad experimental survey articles [117] [118] also document most of these epigenetic DNA repair deficiencies in cancers. Red-highlighted genes are frequently reduced or silenced by epigenetic mechanisms in various cancers. When these genes have low or absent expression, DNA damages can accumulate.
Spore photoproduct lyase (EC 4.1.99.14SP lyase, SPL, SplB, SplG) is a radical SAM enzyme that repairs DNA cross linking of thymine bases caused by UV-radiation.There are several types of thymine cross linking, but SPL specifically targets 5-thyminyl-5,6-dihydrothymine, which is also called spore photoproduct (SP).
Three of these proteins are essential in detecting the mismatch and directing repair machinery to it: MutS, MutH and MutL (MutS is a homologue of HexA and MutL of HexB). MutS forms a dimer (MutS 2 ) that recognises the mismatched base on the daughter strand and binds the mutated DNA.
Melanoma cells are commonly defective in postreplication repair of DNA damages that are in the form of cyclobutane pyrimidine dimers, a type of damage caused by ultraviolet radiation. [11] [12] A particular repair process that appears to be defective in melanoma cells is homologous recombinational repair. [12]
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