A central mechanism in cellular defence against oxidative or electrophilic 
stress is mediated by transcriptional induction of genes via the ARE 
(antioxidant-response element), a cis-acting sequence present in the regulatory 
regions of genes involved in the detoxification and elimination of reactive 
oxidants and electrophiles. The ARE binds different bZIP (basic-region leucine 
zipper) transcription factors, most notably Nrf2 (nuclear factor-erythroid 
2-related factor 2) that functions as a transcriptional activator via 
heterodimerization with small Maf proteins. Although ARE activation by Nrf2 is 
relatively well understood, the mechanisms by which ARE-mediated signalling is 
down-regulated are poorly known. Transcription factor BACH1 [BTB (broad-complex, 
tramtrack and bric-a-brac) and CNC (cap'n'collar protein) homology 1] binds to 
ARE-like sequences, functioning as a transcriptional repressor in a subset of 
ARE-regulated genes, thus antagonizing the activator function of Nrf2. In the 
present study, we have demonstrated that BACH1 itself is regulated by Nrf2 as it 
is induced by Nrf2 overexpression and by Nrf2-activating agents in an 
Nrf2-dependent manner. Furthermore, a functional ARE site was identified at 
+1411 from the transcription start site of transcript variant 2 of BACH1. We 
conclude that BACH1 is a bona fide Nrf2 target gene and that induction of BACH1 
by Nrf2 may serve as a feedback-inhibitory mechanism for ARE-mediated gene 
regulation.