ArticleAmerican journal of physiology. Cell physiology2023
CFTR and PC2, partners in the primary cilia in autosomal dominant polycystic kidney disease.
Article in American journal of physiology. Cell physiology, 2023. 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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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Patient-derived kidney organoids recapitulate ADPKD and facilitate the identification of Rho pathway inhibitors as candidate therapeutics.Cell reports. Medicine · 2026Article
- Sodium-Glucose Cotransporter 2 Inhibitors in Autosomal Dominant Polycystic Kidney Disease: Mechanistic Insights and Therapeutic Promise.Journal of the American Society of Nephrology : JASN · 2026Review
- Review
- Ultrastructure expansion microscopy (U-ExM) of mouse and human kidneys for analysis of subcellular structures.Cytoskeleton (Hoboken, N.J.) · 2024Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Defects in the primary cilium are associated with autosomal dominant polycystic kidney disease (ADPKD). We used a combination of animal models, Western blotting, and confocal microscopy and discovered that CFTR and polycystin 2 (PC2) are both colocalized to the cilium in normal kidneys, with the levels of both being decreased in cystic epithelia. Cilia were longer in CFTR-null mice and in cystic cells in our ADPKD animal models. We examined septin 2, known to play a role in cilia length, to act as a diffusion barrier and to serve as an enhancer of proliferation. We found that septin 2 protein levels were upregulated and colocalized strongly with CFTR in cystic cells. Application of VX-809, the CFTR corrector, restored CFTR and PC2 toward normal in the cilia, decreased the protein levels of septin 2, and drastically reduced septin 2 colocalization with CFTR. Our data suggest that CFTR is present in the cilia and plays a role there, perhaps through its conductance of Cl
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Registered trials
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