The regulation of gene expression in response to environmental signals and 
metabolic imbalances is a key step in maintaining cellular homeostasis. BTB and 
CNC homology 1 (BACH1) is a heme-binding transcription factor repressing the 
transcription from a subset of MAF recognition elements at low intracellular 
heme levels. Upon heme binding, BACH1 is released from the MAF recognition 
elements, resulting in increased expression of antioxidant response genes. To 
systematically address the gene regulatory networks involving BACH1, we combined 
chromatin immunoprecipitation sequencing analysis of BACH1 target genes in HEK 
293 cells with knockdown of BACH1 using three independent types of small 
interfering RNAs followed by transcriptome profiling using microarrays. The 59 
BACH1 target genes identified by chromatin immunoprecipitation sequencing were 
found highly enriched in genes showing expression changes after BACH1 knockdown, 
demonstrating the impact of BACH1 repression on transcription. In addition to 
known and new BACH1 targets involved in heme degradation (HMOX1, FTL, FTH1, ME1, 
and SLC48A1) and redox regulation (GCLC, GCLM, and SLC7A11), we also discovered 
BACH1 target genes affecting cell cycle and apoptosis pathways (ITPR2, CALM1, 
SQSTM1, TFE3, EWSR1, CDK6, BCL2L11, and MAFG) as well as subcellular transport 
processes (CLSTN1, PSAP, MAPT, and vault RNA). The newly identified impact of 
BACH1 on genes involved in neurodegenerative processes and proliferation 
provides an interesting basis for future dissection of BACH1-mediated gene 
repression in neurodegeneration and virus-induced cancerogenesis.