Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2018 Apr 11;83(6):1107–1118. doi: 10.1093/neuros/nyy121

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© Congress of Neurological Surgeons 2018.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence (http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

PMC Copyright notice

FIGURE 2. — Details of the SHH and Akt pathways. Without SHH binding, PTCH1 renders smoothened (SMO) inactive and inhibits it from signaling downstream targets. When SHH binds to PTCH1, SMO is released from this inhibition, allowing it to interact with SUFU. This results in the activation and nuclear translocation of glioma-associated oncogene homologue 1 (GLI1) and (GLI2), and the degradation of GLI3. In the Akt pathway, PTEN normally targets IP3 to inhibit the phosphorylation of Akt. When growth factor (GF) binding to receptor tyrosine kinases (RTK) occurs, PI3K signaling is increased, leading to IP3 accumulation, phosphorylation of Akt and activation of downstream targets.