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.
Ptk7-mediated non-canonical Wnt signaling promotes epithelial plasticity and fluidization, essential for efficient airway epithelial repair post-injury.
Conditional Ptk7 floxed mouse model developed by genOway, enabling epithelial-specific deletion to study non-canonical Wnt signaling in airway repair.
Lung injury repair, Non-canonical Wnt pathway, Airway regeneration, Epithelial dynamics
Conditional Knockout model, Floxed Ptk7 allele, Epithelial-specific Cre, Wnt signaling
From model design to experimental results
Tailor-made solutions adapted to scientific questions
Comprehensive dataset package
Generated with biopharma partners and in-house
Scientific follow-up and advice along the project
Collaborative approach for problem solving and development of innovative models
Breeding facilities in US and Europe
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