ArticleAnimal cells and systems2022
Yap signalling regulates ductular reactions in mice with CRISPR/Cas9-induced glycogen storage disease type Ia.
Article in Animal cells and systems, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 2 citations in OpenAlex.
- Matrix stiffness may drive multi-cellular crosstalk via YAP signaling in biliary atresia liver fibrosis: a mechanistic review.Frontiers in cell and developmental biology · 2026Review
- Generation of a glycogen storage disease mouse model with fatty liver and its treatment by PPAR-α agonist bezafibrate.Frontiers in pharmacology · 2026Article
- Identification of YAP regulators through high-throughput screening and NanoBiT-based validation-drug repositioning for cancer therapy.Animal cells and systems · 2025Article
- Factors affecting the cleavage efficiency of the CRISPR-Cas9 system.Animal cells and systems · 2024Review
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Authors and funding
11 authors at 4 institutions in 1 country.
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Abstract
Glycogen storage disease type Ia (GSD-Ia) is caused by a deficiency in the glucose-6-phosphatase (G6Pase, G6pc) enzyme, which catalyses the final step of gluconeogenesis and glycogenolysis. Accumulation of G6pc can lead to an increase in glycogen and development of fatty liver. Ductular reactions refer to the proliferation of cholangiocytes and hepatic progenitors, which worsen fatty liver progress. To date, however, ductular reactions in GSD-Ia remain poorly understood. Here, we studied the development and potential underlying mechanism of ductular reactions in GSD-Ia in mice. We first generated GSD-Ia mice using CRISPR/Cas9 to target the exon 3 region of the
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