BACH1

BACH1

BACH1: Human BTB and CNC homology 1
PDB Code: 2IHC
Description
BACH1 belongs to the small basic region leucine zipper (bZIP) family Maf of transcriptional activators/repressors. BACH1 contains a BTB (broad complex, tramtrack, bric-a-brac) domain, also known as a POZ (poxvirus and zinc finger) domain. The BTB/POZ domains facilitate protein-protein interactions and formation of homo-and/or heterooligomers. BACH1 is localized in the cytoplasm whereas a shorter isoform (BACH1t) accumulates in the nucleus. Inhibition of heme synthesis enhances nuclear accumulation of BACH1, whereas treatment of cells with hemin results in nuclear exclusion.
BACH1 activity is regulated by oxidation and BACH1 may function as a transcriptional activator or repressor depending on the cellular context. The protein regulates antioxidant enzymes, in particular hemeoxygenase 1 (HO-1), which is an antioxidant defense enzyme that converts toxic heme into antioxidants and is essential for higher eukaryotes in order to cope with various aspects of cellular stress and to regulate cellular iron metabolism.
BACH1 heterodimerises with the basic region leucine zipper (bZip) protein MafK. Complex formation is mediated by its BTB domains and generates multimeric and multivalent DNA binding complexes. In addition, BACH1 dimerizes with its shorter isoform BACH1t resulting in nuclear import of BACH1.
BACH1 knock-out mice are viable and fertile and appear grossly normal in size and morphology. However, BACH1 -/- mice have constitutive high expression of HO-1 in various tissues under normal physiological conditions (uncoupled from stress-responsive control) and are resistant to pro-atherosclerotic and ischemic stresses. In addition, smooth muscle cell proliferation is reduced in BACH1 -/- mice.
Transgenic mice expressing human BACH1 under the control of GATA-1 show significant thrombocytopenia associated with impaired maturation of megakaryocytes and reduced proplatelet formation. The modal ploidy class of megakaryocytes in these mice was 2N, indicating impairment of endomitosis. In addition these transgenic mice develop myelofibrosis and show a down-regulated transcription of the p45 target genes.
BACH1 plays critical roles in the regulation of macrophages and SMC functions and pathogenesis of atherosclerosis and is a potential target for antiatherosclerotic /antiinflammatory therapy. Aberrant BACH1 expression has been reported in brains of fetuses with Down syndrome and patients with Down syndrome and Alzheimer’s disease.

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