The V-maf musculoaponeurotic fibrosarcoma oncogene homolog K (MAFK) is a member of the Maf family of transcription factors. These proteins play crucial roles in various biological processes, including cellular differentiation, proliferation, and apoptosis. The MAFK gene is particularly significant in the context of cancer research due to its involvement in oncogenesis.
The Maf family of transcription factors was first identified in the genome of the avian transforming retrovirus AS42. The v-Maf oncogene was found to cause musculoaponeurotic fibrosarcoma in vivo and could transform chicken embryo fibroblasts in vitro . The term “v-Maf” refers to the viral form of the gene, while “c-Maf” refers to the cellular counterpart.
MAFK, like other Maf proteins, belongs to the basic leucine zipper (bZIP) family of transcription factors. These proteins function by binding to specific DNA sequences and regulating the expression of target genes. MAFK is known to form both homodimers and heterodimers with other bZIP proteins, influencing a wide range of cellular activities.
MAFK has been implicated in various types of cancer, including musculoaponeurotic fibrosarcoma, a rare type of soft tissue sarcoma. Overexpression of MAFK can lead to uncontrolled cell proliferation and tumor formation. Research has shown that MAFK overexpression is efficient and sufficient to induce β-cell differentiation and insulin secretion from human pancreatic duct-derived cells (HDDCs), allowing the cells to mitigate hyperglycemia in diabetic SCID-beige mice .
The ability of MAFK to induce β-cell differentiation has significant implications for diabetes treatment. β-cell replacement therapy represents a promising approach to restore glucose homeostasis in patients with type 1 diabetes. Studies have demonstrated that synthetic modified mRNA for MAFK can drive the reprogramming of HDDCs into insulin-secreting cells, offering a potential new avenue for diabetes therapy .