Recombinant Human BACH1.3 protein

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

The BACH1.3 gene encodes a transcription regulator protein also known as BTB and CNC homology 1 basic leucine zipper transcription factor 1. The protein weighs approximately 105 kDa and you can find it in various tissues including the liver lungs and kidneys. It binds to the antioxidant response elements (ARE) in DNA regulating the transcription of genes involved in oxidative stress response. BACH1.3 functions by repressing gene activation through heterodimerization with small Maf proteins which helps maintain cellular redox balance.

Biological function summary

BACH1.3 modulates gene expression by forming complexes with small Maf proteins which are necessary for its regulatory activity. This protein plays a role in cellular oxidative stress management and heme metabolism. Through its function in stress response regulation BACH1.3 influences the expression of several genes such as heme oxygenase-1 (HO-1) important for detoxifying reactive oxygen species. By controlling these pathways BACH1.3 supports cell protection and adaptation to environmental oxidative stress.

Pathways

BACH1.3 participates in the oxidative stress response and heme degradation pathways. It partners with the KEAP1-NRF2 pathway where it acts as a negative regulator of NRF2 target genes by competing with NRF2 for binding to ARE sequences. This action impacts the transcription of antioxidant genes. BACH1.3 indirectly affects the expression of proteins like HO-1 and NAD(P)H:quinone oxidoreductase 1 (NQO1) moderating their protective effects in the cell.

Altered BACH1.3 function associates with cancer and cardiovascular diseases. Its involvement in improper oxidative stress response can lead to tumor progression and resistance to therapeutic agents in some cancers. Additionally in cardiovascular diseases BACH1.3 connects to abnormal arterial remodeling due to its regulation of genes involved in oxidative stress. This target interacts with proteins like KEAP1 and NRF2 modifying disease outcomes through changes in redox-sensitive signaling and gene expression.