Ingridjordens
@ingridjordens.bsky.social
Cell biologist | Wnt signaling | Stem cells | Center for Molecular Medicine | University Medical Center Utrecht | madelonmauricelab.nl
Reposted by Ingridjordens
Excited about our pre-print on AXIN1 mutations in HCC!
We found that AXIN1 mutations drive low but physiologically relevant levels of Wnt/β-catenin signaling, while being permissive to YAP/TAZ activation. This helps explain why mutations in AXIN1 and β-catenin are linked to distinct HCC subtypes.
We found that AXIN1 mutations drive low but physiologically relevant levels of Wnt/β-catenin signaling, while being permissive to YAP/TAZ activation. This helps explain why mutations in AXIN1 and β-catenin are linked to distinct HCC subtypes.
Hepatocellular carcinoma-associated AXIN1 mutations drive low levels of Wnt/β-catenin pathway activity that allow for niche-independent growth and YAP/TAZ signaling https://www.biorxiv.org/content/10.1101/2024.11.28.625941v1
Hepatocellular carcinoma-associated AXIN1 mutations drive low levels of Wnt/β-catenin pathway activity that allow for niche-independent growth and YAP/TAZ signaling https://www.biorxiv.org/content/10.1101/2024.11.28.625941v1
In healthy cells, AXIN1 organizes assembly of a large destruction complex that mediates proteolysis
www.biorxiv.org
December 8, 2024 at 4:17 PM
Excited about our pre-print on AXIN1 mutations in HCC!
We found that AXIN1 mutations drive low but physiologically relevant levels of Wnt/β-catenin signaling, while being permissive to YAP/TAZ activation. This helps explain why mutations in AXIN1 and β-catenin are linked to distinct HCC subtypes.
We found that AXIN1 mutations drive low but physiologically relevant levels of Wnt/β-catenin signaling, while being permissive to YAP/TAZ activation. This helps explain why mutations in AXIN1 and β-catenin are linked to distinct HCC subtypes.