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. 2020 Dec 11;477(23):4603–4621. doi: 10.1042/BCJ20200506

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© 2020 The Author(s)

This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY). Open access for this article was enabled by the participation of University of Oxford in an all-inclusive Read & Publish pilot with Portland Press and the Biochemical Society under a transformative agreement with JISC.

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Figure 5. — In the absence of hedgehog (Hh) ligands, the Hh receptor PTCH associates with SMO to inhibit SMO function. The GLI2/3 transcription factors are held in complex by a primary cilium-localized inhibitory complex consisting of the kinases CK1, GSK3 and PKA. Following GLI2/3 phosphorylation by CK1, GSK3 and PKA, GLI2/3 is marked for proteasomal degradation. In the presence of Hh ligands, SMO is released from PTCH and is free to mediate the release of GLI2/3 from the inhibitory kinase complex. GLI2/3 can now translocate to the nucleus and induce Hh target gene transcription. CK1 and GRK2 have been reported to phosphorylate SMO to promote full SMO activation and maximal release of GLI2/3 from the inhibitory complex.