Nucleotide excision repair is the mechanism of DNA repair. The other mutations cause chemical (ie, intercalating agent), and radiation, DNA damage occurs steadily. DNA mismatch repair nucleotide excision repair (NER), base excision repair and (BER), (MMR): Three excision repair pathway exists to repair the damage to the single-stranded DNA. it is possible paths BER recognizes the non-bulky lesions specific DNA, but it is a base that is damaged, can be adjusted is removed by a specific glycosylase. Similarly, the way the MMR, non-Watson – to target Crick base pairing.
Nucleotide excision repair (NER), resection removal mechanism is particularly important mutations caused by UV-induced DNA damage. UV result in DNA damage in DNA adducts and bulky – these adducts, 6,4 and thymine dimer mainly – is light product. Recognition removal injury results in short single-stranded DNA segment lesions are included. It remains intact single-stranded DNA, DNA polymerase is used as a template for the synthesis of short complementary sequence. Forming ligation full Neil final, the double DNA, but is carried out by DNA ligase. I can NER is divided into 2 subpathways: link global genome transcription and NER NER (GG-NER) and (TC-NER). How to recognize DNA damage is different from both subpathways them, but they have the same method of ligation and repair of the lesion incision. The importance of NER has been evidenced by the severe human disease is the result of a genetic mutation that was born of the NER protein. Cockayne syndrome and xeroderma pigmentosum are two examples of diseases associated with Abner.
Since its inception, life, is facing a major problem that forms stored genetic information it is not chemically inert. DNA integrity is challenged impair its function, the harmful effects of physical factors and chemical plurality. In order to protect the Achilles tendon, a complex network of systems for DNA repair is done at the beginning of evolution. Versatile to counteract the deleterious effects of DNA damage including many basic types of induced damage nucleotide excision repair (NER), by environmental information source, one is the removal pathway of DNA damage that has been refined. The lesions most suitable under the panel, there are two main types of the victim that was generated by the short-wave UV light component product cyclobutane pyrimidine dimers and (CPD), of sunlight. Furthermore, chemical adducts bulky Many are removed by this process. Among the diverse spectrum of NER lesions, significant distortion of the helix of the DNA is common. Has been observed prototype repair syndrome xeroderma pigmentosum in (XP) the NER defect underlying the high sensitive predisposition to skin cancer. Represents repair genesXPA-G with different seven XP complementation group were identified.
Over the past decade, a major factor of all Neil has been cloned basis of the reaction of the “cut and paste” is dissolved in the in vitro from purified components. Recently, XPC has been identified as a repair factor recruitment to DNA damage sensor (complex with hHR23B). And a transcription factor TFIIH complex common with the separation of the intermediary chain and XPD helicase XPB, the lesion site. Check the damage found in the DNA structure, XPA is extremely important for the assembly of the rest of the repair mechanism. The (RPA), to stabilize the open DNA complex, ERCC1 and XPG, replication protein is involved in the positioning of responsibility XPF endonuclease incision of the DNA around the lesion. After removing the damaged containing oligonucleotide is 24-32 nucleotides, in order to close it, the length is a duplicate of the same factors fill the remaining gap in general.
Able to distinguish between two modes of channel you can: repair of damage on the genome all, because block transcription repair the lesions present in the DNA strand that has been transferred global genome NER and (GG-NER), transcription-coupled NER (TC called – NER). Defects of XP group harbor the most common component of both subpathways of NER. GG-NER is dependent on the activity of the factor of all of the above, including complex XPC-hHR23B of GG-NER-specific. Cost of repair of GG-NER for is highly dependent on the type of lesion. For example, the difference in affinity of the damage sensor XPC-hHR23B, perhaps, from the genome of CPD, 6 4PPs is removed much faster. In addition, the location of the lesion (access) can affect the removal rate in the in vivo. The TC-NER, damage is detected by extending the RNA polymerase II complex when it detects a lesion. Interestingly, significant failure, Cockayne syndrome is associated with a specific defect in transcription-coupled repair. Determination of (CS-B and CS-A) 2 complementation groups, indicating that it is particularly necessary for the repair quickly and efficiently strands gene product two is transferred at least.
Phenotype, CS tough and sensitive, it is a condition to be very versatile in terms characterized by premature aging and features of neuronal development,. Most of these symptoms, it is not seen even in NER-deficient XP patients in general. CS protein and transcription-coupled repair and / or show that you have a function outside the NER is further symptoms of CS. also that the binding of polymerase transcription elongation failure to block multiple pathways for repair, seems to be removed in transcription-coupled manner (such as oxidative damage, for example) non-NER lesions. Interestingly, the display function of the XP-G CS patients in combination with symptoms XP XP-B some, and XP-D,. However, people of XP-D and XP-C of the other suffer as CS-hair syndrome trichothiodystrophy brittle. This clinical challenge and point to the role of additional NER factors of these. The TTD mouse model is a mutation associated with XPD subdivision of the dual function complex TFIIH with basal transcription defects in the base of the TTD at least some of the events recently. Thus, associated with the heterogeneity of clinical surprisingly high for the additional features of the factors NER defects are involved Abner.