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The interaction between HIV-1 integrase and Ku70 facilitates postintegrational DNA repairтезисы доклада Тезисы
Информация о цитировании статьи получена из
Web of Science
Дата последнего поиска статьи во внешних источниках: 22 февраля 2019 г.
- Авторы: Anisenko A., Knyazhanskaya E., Zatsepin T., Gottikh M.
- Сборник: FEBS Open Bio
- Серия: Supplement 1
- Том: 8
- Тезисы
- Год издания: 2018
- Место издания: FEBS Open Bio Prague, Czech Republic
- Первая страница: 202
- Последняя страница: 203
- DOI: 10.1002/2211-5463.12453
- Аннотация: The integration of the HIV DNA into the host genome is completed by cellular factors that repair the short gaps flanking the proviral DNA. We have shown earlier, that viral integrase can directly interact with Ku70 repair factor, and this interaction is weakened by E212A/L213A substitutions in integrase. The transduction of HEK 293T cells by a singleround HIV1 vector is found to be decreased in cells stably depleted of the DNAPK repair components (Ku70, Ku80 or DNAPKcs). We have established a qPCRbased approach for quantitative measurement of postintegrational gap repair and shown that depletion of any DNAPK component reduces gaprepair efficiency in our system. The same effects have been detected in presence of specific DNAPKcs inhibitor Nu7441. Viral vector carrying E212A/L213A integrase substitutions demonstrates decreased gaprepair and a reduced sensitivity to the DNA-PK components depletion while its integrational capacity remains at the wildtype level. We speculate that integrase recruits DNAPK complex to gap cites and facilitates gaprepair through a direct interaction with Ku70 subunit. This work was supported by RFBR grant 1704 01178 and RSF grant 17141107 (development of the gap repair approach).
- Добавил в систему: Анисенко Андрей Николаевич