Non-canonical Wnt signaling promotes epithelial fluidization in the repairing airway

Jun-Kit Hu D
Genentech
May 3, 2025
Nat Commun
https://pubmed.ncbi.nlm.nih.gov/40319020

This article is currently being updated. View its version on PubMed.

https://pubmed.ncbi.nlm.nih.gov/40319020

Research summary

This study reveals the role of non-canonical Wnt signaling in regulating epithelial fluidization during airway repair. The authors show that Wnt signaling via Ptk7 promotes a dynamic, migratory epithelial state after injury. Using a conditional Ptk7 knockout mouse model, they demonstrate that loss of Ptk7 impairs epithelial fluidization, delays wound closure, and disrupts proper airway regeneration.

Key outcome of the study

Ptk7-mediated non-canonical Wnt signaling promotes epithelial plasticity and fluidization, essential for efficient airway epithelial repair post-injury.

Mouse model

Conditional Ptk7 floxed mouse model developed by genOway, enabling epithelial-specific deletion to study non-canonical Wnt signaling in airway repair.

TARGET:
Ptk7
Protein Tyrosine Kinase 7, Colon Carcinoma Kinase-4 (CCK-4)

Keywords

Lung injury repair, Non-canonical Wnt pathway, Airway regeneration, Epithelial dynamics

Technical specifications

Conditional Knockout model, Floxed Ptk7 allele, Epithelial-specific Cre, Wnt signaling

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KO repository

>2000 conditional Knockout mouse models for target discovery and  confirmation, in vivo compound specificity, MOA, and clinical studies

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