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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

GSK3beta positively regulates Hedgehog signaling through Sufu in mammalian cells.

Hedgehog signaling plays important roles in embryonic patterning of multicellular organisms. This pathway is ultimately transmitted by the zinc-finger transcriptional factor Gli, of which activity is suppressed by Sufu, a negative regulator of this signaling. To clarify this regulation to more detail, we screened for Sufu-binding proteins. We identified GSK3beta as a specific binding partner of Sufu by mass spectrometric analysis. GSK3beta bound to Sufu both in vitro and in vivo. Down-regulation of GSK3beta expression by RNAi in Hedgehog-responsive cells attenuated Hedgehog signaling, suggesting that GSK3beta functions as a positive regulator of Hedgehog signaling. In addition, an in vitro kinase assay showed that GSK3beta phosphorylates Sufu and phosphorylation-mimicking mutant of Sufu showed significantly decreased ability to bind Gli1 and could not suppress the Gli-mediated expression of a reporter gene efficiently. These results strongly suggest that GSK3beta phosphorylates Sufu to positively regulate Hedgehog signaling in mammalian cells.[1]


  1. GSK3beta positively regulates Hedgehog signaling through Sufu in mammalian cells. Takenaka, K., Kise, Y., Miki, H. Biochem. Biophys. Res. Commun. (2007) [Pubmed]
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