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. 2015 Nov 30;4(11):e176. doi: 10.1038/oncsis.2015.38

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Copyright © 2015 Macmillan Publishers Limited

Oncogenesis is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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A model representing the positive feedback loop formed by Hck and Gli1 in activating Shh target genes. Active Gli1 in response to Shh signaling induces the expression of Shh target genes including Hck, which encodes a tyrosine kinase that could enhance Gli1 transcription activator functions. Hck disrupts the interaction between Gli1 and its inhibitor Sufu, possibly through Hck–Gli1 interactions. Hck could phosphorylate Gli1 and the Tyr phosphorylation of Gli1 further enhances the Gli1 activities. Thus the positive feedback loop formed by Hck and Gli1 amplifies Shh signaling outputs.