Anton Venhuizen
@antonvenhuizen.bsky.social
Postdoc in Wnt signalling @Gammons lab @CIMR
I had an amazing week full of great talks and discussions at the Gordon Research Seminar and Conference on Wnt signalling in Maine, US. I also had the honour of leading the GRS panel discussion and was selected to present work from the Gammons lab during the GRC. Many thanks to the organisers!
July 2, 2025 at 10:51 PM
I had an amazing week full of great talks and discussions at the Gordon Research Seminar and Conference on Wnt signalling in Maine, US. I also had the honour of leading the GRS panel discussion and was selected to present work from the Gammons lab during the GRC. Many thanks to the organisers!
Reposted by Anton Venhuizen
Yesterday, @antonvenhuizen.bsky.social successfully defended his thesis "Molecular mechanisms of the
β-catenin destruction complex in health and disease", which describes the versatile field of WNT regulator AXIN1.
We are super proud and wish Dr. Venhuizen all the best in Cambridge!
β-catenin destruction complex in health and disease", which describes the versatile field of WNT regulator AXIN1.
We are super proud and wish Dr. Venhuizen all the best in Cambridge!
May 8, 2025 at 7:39 AM
Yesterday, @antonvenhuizen.bsky.social successfully defended his thesis "Molecular mechanisms of the
β-catenin destruction complex in health and disease", which describes the versatile field of WNT regulator AXIN1.
We are super proud and wish Dr. Venhuizen all the best in Cambridge!
β-catenin destruction complex in health and disease", which describes the versatile field of WNT regulator AXIN1.
We are super proud and wish Dr. Venhuizen all the best in Cambridge!
Reposted by Anton Venhuizen
Our first selected oral presentation comes from Elisabeth Chapman from the @melissa-gammons1.bsky.social group at the CIMR @thecimr.bsky.social telling us about her research into casein kinase 1 regulation of Wnt signalosome assembly.
#WNTUK2025
#WNTUK2025
March 24, 2025 at 10:45 AM
Our first selected oral presentation comes from Elisabeth Chapman from the @melissa-gammons1.bsky.social group at the CIMR @thecimr.bsky.social telling us about her research into casein kinase 1 regulation of Wnt signalosome assembly.
#WNTUK2025
#WNTUK2025
Reposted by Anton Venhuizen
Hello! Although we are still in the other place, this will become our main social media feed. We're part of the University of Cambridge Clinical School
Cell biology, molecular mechanisms of human disease
Cell biology, molecular mechanisms of human disease
January 16, 2025 at 10:50 AM
Hello! Although we are still in the other place, this will become our main social media feed. We're part of the University of Cambridge Clinical School
Cell biology, molecular mechanisms of human disease
Cell biology, molecular mechanisms of human disease
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.