ArticleHuman molecular genetics2016
Reduction of ciliary length through pharmacologic or genetic inhibition of CDK5 attenuates polycystic kidney disease in a model of nephronophthisis.
Article in Human molecular genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
32 citing papers in PubMed, 50 citations in OpenAlex.
- Disruption of primary ciliary prostaglandin EJournal of biomedical science · 2026Article
- Ciliary-Mediated Mechanotransduction in Skeletal Development and Diseases.Results and problems in cell differentiation · 2026Review
- Prostaglandin E2 and Progesterone Receptor Coordinately Regulate Primary Cilia for Proper Decidualization.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Post-Translational Modifications in Cilia and Ciliopathies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Review
- Agonists of prostaglandin EProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Manipulation of the Tubulin Code Alters Directional Cell Migration and Ciliogenesis.Frontiers in cell and developmental biology · 2022Article
- TFP5-Mediated CDK5 Activity Inhibition Improves Diabetic NephropathyFrontiers in cell and developmental biology · 2022Article
- Epithelial proliferation and cell cycle dysregulation in kidney injury and disease.Kidney international · 2021Review
- Quinomycin A reduces cyst progression in polycystic kidney disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Intraflagellar Transport Proteins as Regulators of Primary Cilia Length.Frontiers in cell and developmental biology · 2021Review
- Renal Ciliopathies: Sorting Out Therapeutic Approaches for Nephronophthisis.Frontiers in cell and developmental biology · 2021Review
- Exploring the Spectrum of Kidney Ciliopathies.Diagnostics (Basel, Switzerland) · 2020Review
- Correction of cilia structure and function alleviates multi-organ pathology in Bardet-Biedl syndrome mice.Human molecular genetics · 2020Article
- Disease Modeling To Understand the Pathomechanisms of Human Genetic Kidney Disorders.Clinical journal of the American Society of Nephrology : CJASN · 2020Review
- Role of cyclin-dependent kinase 2 in the progression of mouse juvenile cystic kidney disease.Laboratory investigation; a journal of technical methods and pathology · 2020Article
- Primary Cilia, Ciliogenesis and the Actin Cytoskeleton: A Little Less Resorption, A Little More Actin Please.Frontiers in cell and developmental biology · 2020Review
- Therapeutic perspectives for structural and functional abnormalities of cilia.Cellular and molecular life sciences : CMLS · 2019Review
- LF4/MOK and a CDK-related kinase regulate the number and length of cilia in Tetrahymena.PLoS genetics · 2019Article
- Analysis of primary cilia in renal tissue and cells.Methods in cell biology · 2019Article
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 2 countries.
Funding
Abstract
Polycystic kidney diseases (PKDs) comprise a subgroup of ciliopathies characterized by the formation of fluid-filled kidney cysts and progression to end-stage renal disease. A mechanistic understanding of cystogenesis is crucial for the development of viable therapeutic options. Here, we identify CDK5, a kinase active in post mitotic cells, as a new and important mediator of PKD progression. We show that long-lasting attenuation of PKD in the juvenile cystic kidneys (jck) mouse model of nephronophthisis by pharmacological inhibition of CDK5 using either R-roscovitine or S-CR8 is accompanied by sustained shortening of cilia and a more normal epithelial phenotype, suggesting this treatment results in a reprogramming of cellular differentiation. Also, a knock down of Cdk5 in jck cells using small interfering RNA results in significant shortening of ciliary length, similar to what we observed with R-roscovitine. Finally, conditional inactivation of Cdk5 in the jck mice significantly attenuates cystic disease progression and is associated with shortening of ciliary length as well as restoration of cellular differentiation. Our results suggest that CDK5 may regulate ciliary length by affecting tubulin dynamics via its substrate collapsin response mediator protein 2. Taken together, our data support therapeutic approaches aimed at restoration of ciliogenesis and cellular differentiation as a promising strategy for the treatment of renal cystic diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.