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Kaneto, H. et al.

Hideaki Kaneto, Taka-Aki Matsuoka, Satoshi Kawashima, Kaoru Yamamoto, Ken Kato, Takeshi Miyatsuka, Naoto Katakami, Munehide Matsuhisa,

Role of MafA in pancreatic beta-cells.

Pancreatic beta-cell-specific insulin gene expression is regulated by a variety of pancreatic transcription factors and the conserved A3, C1 and E1 elements in the insulin gene enhancer region are very important for activation of insulin gene. Indeed, PDX-1 binding to the A3 element and NeuroD binding to the E1 element are crucial for insulin gene transcription. Recently, C1 element-binding transcription factor was identified as MafA, which is a basic-leucine zipper transcription factor and functions as a potent transactivator for the insulin gene. Under diabetic conditions, chronic hyperglycemia gradually deteriorates pancreatic beta-cell function, which is accompanied by decreased expression and/or DNA binding activities of MafA and PDX-1. Furthermore, MafA overexpression, together with PDX-1 and NeuroD, markedly induces insulin biosynthesis in various non-beta-cells and thereby is a useful tool to efficiently induce insulin-producing surrogate beta-cells. These results suggest that MafA plays a crucial role in pancreatic beta-cells and could be a novel therapeutic target for diabetes.[1]

References

Role of MafA in pancreatic beta-cells. Kaneto, H., Matsuoka, T.A., Kawashima, S., Yamamoto, K., Kato, K., Miyatsuka, T., Katakami, N., Matsuhisa, M. Adv. Drug Deliv. Rev. (2009) [Pubmed]

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