Disease relevance of Bach2

• The Bach2-enhanced green fluorescent protein bicistronic retrovirus was used to monitor the fate of Bach2-expressing cells at the single cell level [1].
• Bach2 is involved in neuronal differentiation of N1E-115 neuroblastoma cells [2].

High impact information on Bach2

• Bach2 is a B-cell- and neuron-specific transcription repressor that forms heterodimers with the Maf-related oncoproteins [3].
• In transfection assays using fibroblast cells, the fgf4 gene was upregulated in the presence of both MAZR and Bach2 in a BTB/POZ domain-dependent manner [3].
• A combinatorial code for gene expression generated by transcription factor Bach2 and MAZR (MAZ-related factor) through the BTB/POZ domain [3].
• MAZR forms homo- and hetero-oligomers with Bach2 through the BTB domain, which oligomers bind to guanine-rich sequences [3].
• Bach1 and Bach2 function as transcription repressors in transfection assays using fibroblast cells, but they function as a transcriptional activator and repressor, respectively, in cultured erythroid cells [4].

Biological context of Bach2

• The fgf4 gene, which regulates morphogenesis of limb buds, contains both guanine-rich sequences and a Bach2 binding site in its regulatory region [3].
• Bach2 exerted an inhibitory effect on NIH3T3 cell proliferation and caused massive apoptosis upon mild oxidative stress in both NIH3T3 and Raji B-lymphoid cells [1].
• Although both oxidative stress and leptomycin B, an inhibitor of nuclear export, induce nuclear accumulation of Bach2, the leptomycin B-induced nuclear accumulation of Bach2 was not sufficient to elicit apoptosis [1].
• Activation of Maf/AP-1 repressor Bach2 by oxidative stress promotes apoptosis and its interaction with promyelocytic leukemia nuclear bodies [1].
• Our results suggest that Bach2 constitutes a cell lineage-specific system that couples oxidative stress and cell death and that inhibition of 12-O-tetradecanoylphorbol-13-acetate response element, the Maf recognition element, and the antioxidant-responsive element upon oxidative stress may be critical determinants for apoptosis [1].

Anatomical context of Bach2

• Consistent with the fact that subcellular localization of Bach2 is regulated by nuclear export in cultured cells, extensive Bach2-staining was found in the cytoplasmic regions of developing neuronal and lens cells [5].
• Little is known about the direct target genes of Bach2 in B cells [6].
• Therefore, the Prdm1 regulation in B cells involves the repression by Bach2, which may be cancelled upon terminal plasma cell differentiation [6].

Associations of Bach2 with chemical compounds

• Induction of Prdm1 was more robust and faster in primary Bach2-deficient B cells than in wild-type control B cells upon lipopolysaccharide stimulation [6].

Physical interactions of Bach2

• The heterodimer of Bach2/MafK bound to the Maf recognition element located upstream of the Prdm1 promoter in an electrophoretic mobility shift assay [6].

Regulatory relationships of Bach2

• These results suggest that Bach2 regulates AP-1- and Maf-dependent gene expression during development of neuronal and lens cells and that its activity may be regulated by nuclear export in these cells [5].

Other interactions of Bach2

• Bach2 was induced upon neuronal differentiation of P19 embryonic carcinoma cells, while its related factor Bach1 did not show significant change [5].
• Upon oxidative stress, Bach2 formed nuclear foci that associated with promyelocytic leukemia nuclear bodies [1].

Analytical, diagnostic and therapeutic context of Bach2

• The largest average increase was observed for the transcription factor Bach2, and this increase was confirmed by RT-PCR [7].

References