genes sMafs regulate different target genes depending on their partners. For instance, the p45-NF-E2-sMaf heterodimer regulates genes responsible for platelet production. Although it has not been confirmed by mouse genetic studies, many studies suggest that p45-NFE2-sMaf heterodimer is involved in the regulation of β-globin and other erythroid-related genes. Nrf2-sMaf heterodimer regulates a battery of cytoprotective genes, such as antioxidant/xenobiotic metabolizing enzyme genes. The Bach1-sMaf heterodimer regulates the heme oxygenase-1 gene. The contribution of individual sMafs to the transcriptional regulation of their target genes has not yet been well examined. Disease linkage Loss of sMafs results in disease-like phenotypes as summarized in table below. Mice lacking MafK are seemingly healthy under laboratory conditions, while mice lacking MafG exhibit mild neuronal phenotype and mild thrombocytopenia. However, mice lacking Mafg and one allele of Mafk (Mafg−/−::Mafk+/−) exhibit progressive neuronal degeneration, thrombocytopenia and cataract, and mice lacking MafG and MafK (Mafg−/−::Mafk−/−) exhibit more severe neuronal degeneration and die in the perinatal stage. Mice lacking MafF, MafG and MafK are embryonic lethal. Embryonic fibroblasts that are derived from Maff−/−::Mafg−/−::Mafk−/− mice fail to activate Nrf2-dependent cytoprotective genes in response to stress. In addition, accumulating evidence suggests that as partners of CNC and Bach proteins, sMafs are involved in the onset and progression of various human diseases, including neurodegeneration, arteriosclerosis and cancer. Notes References Further reading External links Transcription factors