The small MAFs, MAFF, MAFG and MAFK have emerged as crucial regulators of mammalian gene expression. Previous studies have linked small MAF function, by virtue of their heterodimerization with the Cap 'n' Collar (CNC) family of transcription factors, to the stress response and detoxification pathways. Recent analyses have revealed a complex regulatory network involving small MAF transcription factors and other cellular proteins. The expression and activity of small MAFs are tightly regulated at multiple levels. With regard to their clinical importance, small MAFs have been linked to various diseases, such as diabetes, neuronal disorders, thrombocytopenia and carcinogenesis. A better understanding of the molecular mechanisms governing the activity of small MAFs will provide novel insights into the control of mammalian transcription and may lead to the development of novel therapeutic strategies to treat common human disorders.
Background: NFE2L3 is involved in carcinogenesis, stress response, differentiation, and inflammatory processes. Results: NFE2L3 is polyubiquitinated via the E3 ubiquitin ligase FBW7, which regulates its turnover. This process requires prior phosphorylation by GSK3. Conclusion: NFE2L3 is tightly regulated by FBW7 and GSK3 through polyubiquitination. Significance: Our data highlight the regulation of NFE2L3 by FBW7 and GSK3 and its potential role in cellular stress response.
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