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Regulation of HIF-1$\upalpha$ activity by overexpression of thioredoxin is independent of thioredoxin reductase statusстатья
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: 26 декабря 2018 г.
- Авторы: Naranjo-Suarez Salvador, Carlson Bradley A., Tobe Ryuta, Yoo Min-Hyuk, Tsuji Petra A., Gladyshev Vadim N., Hatfield Dolph L.
- Журнал: Molecules and Cells
- Том: 36
- Номер: 2
- Год издания: 2013
- Издательство: Springer Verlag
- Местоположение издательства: Germany
- Первая страница: 151
- Последняя страница: 157
- DOI: 10.1007/s10059-013-0121-y
- Аннотация: Under hypoxic conditions, cells activate a transcriptional response mainly driven by hypoxia-inducible factors (HIFs). HIF-1α stabilization and activity are known to be regulated by thioredoxin 1 (Txn1), but how the thioredoxin system regulates the hypoxic response is unknown. By examining the effects of Txn1 overexpression on HIF-1α function in HeLa, HT-29, MCF-7 and EMT6 cell lines, we found that this oxidoreductase did not stabilize HIF-1α, yet could increase its activity. These effects were dependent on the redox function of Txn1. However, Txn1 deficiency did not affect HIF-1α hypoxic-stabilization and activity, and overexpression of thioredoxin reductase 1 (TR1), the natural Txn1 reductase, had no influence on HIF-1α activity. Moreover, overexpression of Txn1 in TR1 deficient HeLa and EMT6 cells was still able to increase HIF-1α hypoxic activity. These results indicate that Txn1 is not essential for HIF-1α hypoxic stabilization or activity, that its overexpression can increase HIF-1α hypoxic activity, and that this effect is observed regardless of TR1 status. Thus, regulation of HIF-1α by the thioredoxin system depends on the specific levels of this system’s major components.
- Добавил в систему: Гладышев Вадим Николаевич