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. 2020 Jan 29;10(2):233–248. doi: 10.1007/s13555-020-00355-1

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License, which permits any non-commercial use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc/4.0/.

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Fig. 3 — Hedgehog pathway activation through the primary cilium. When the Hedgehog pathway is off, patched (PTCH1) localizes to the primary cilium and prevents Smoothened (SMO) from entering the cilium. Simultaneously, suppressor of fused homolog (SUFU) binds to and inhibits the activity of glioma-associated oncogene homolog (GLI) transcription factors. Hedgehog ligands (HH) activate the pathway by binding to PTCH1, causing it to leave the cilium, and allowing SMO to enter. SMO in turn activates GLI proteins, allowing for the transcription of Hedgehog target genes