Proteasomal regulation of HNF4 alpha protein by hypoxia in pancreatic beta-cells.

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HNF4 alpha, a beta-cell transcriptional factor, is a key molecule for insulin secretion from pancreatic beta-cells. Although we found that HNF4 alpha protein was significantly reduced by hypoxia, its molecular mechanism was unclear so far. In this study, we demonstrated that hypoxia-induced activation of AMPK suppresses HNF4 alpha protein levels not via transcriptional regulation, but via ubiquitin-proteasome pathway mediated degradation in vitro. Further experiments are needed to see whether HNF4 alpha protein might be reduced by hypoxia or AMPK activators in vivo.