An internal ribosomal entry site mediates redox-sensitive translation of Nrf2.

ABSTRACT: Nrf2 plays pivotal roles in coordinating the antioxidant response and maintaining redox homeostasis. Nrf2 expression is exquisitely regulated; Nrf2 expression is suppressed under unstressed conditions but strikingly induced under oxidative stress. Previous studies showed that stress-induced Nrf2 up-regulation results from both the inhibition of Nrf2 degradation and enhanced Nrf2 translation. In the present study, we elucidate the mechanism underlying translational control of Nrf2. An internal ribosomal entry site (IRES) was identified within the 5' untranslated region of human Nrf2 mRNA. The IRES(Nrf2) contains a highly conserved 18S rRNA binding site (RBS) that is required for internal initiation. This IRES(Nrf2) also contains a hairpin structured inhibitory element (IE) located upstream

SUBMITTER: Li W 

PROVIDER: S-EPMC2817467 | biostudies-literature | 2010 Jan

REPOSITORIES: biostudies-literature