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Clustered DNA Lesions Containing 5-Formyluracil and AP Site: Repair via the BER Systemстатья
Статья опубликована в высокорейтинговом журнале
Информация о цитировании статьи получена из
Web of Science,
Scopus
Статья опубликована в журнале из списка Web of Science и/или Scopus
Дата последнего поиска статьи во внешних источниках: 24 октября 2013 г.
- Авторы: Belousova Ekaterina A., Vasil'eva Inna A., Moor Nina A., Zatsepin Timofey S., Oretskaya Tatiana S., Lavrik Olga I.
- Журнал: PLoS ONE
- Том: 8
- Номер: 8
- Год издания: 2013
- Издательство: Public Library of Science
- Местоположение издательства: United States
- Первая страница: e68576
- DOI: 10.1371/journal.pone.0068576
- Аннотация: Lesions in the DNA arise under ionizing irradiation conditions or various chemical oxidants as a single damage or as part of a multiply damaged site within 1-2 helical turns (clustered lesion). Here, we explored the repair opportunity of the apurinic/apyrimidinic site (AP site) composed of the clustered lesion with 5-formyluracil (5-foU) by the base excision repair (BER) proteins. We found, that if the AP site is shifted relative to the 5-foU of the opposite strand, it could be repaired primarily via the short-patch BER pathway. In this case, the cleavage efficiency of the AP site-containing DNA strand catalyzed by human apurinic/apyrimidinic endonuclease 1 (hAPE1) decreased under AP site excursion to the 3'-side relative to the lesion in the other DNA strand. DNA synthesis catalyzed by DNA polymerase lambda was more accurate in comparison to the one catalyzed by DNA polymerase beta. If the AP site was located exactly opposite 5-foU it was expected to switch the repair to the long-patch BER pathway. In this situation, human processivity factor hPCNA stimulates the process.
- Добавил в систему: Зацепин Тимофей Сергеевич