ArticleProceedings of the National Academy of Sciences of the United States of America2003
Kidney-specific inactivation of the KIF3A subunit of kinesin-II inhibits renal ciliogenesis and produces polycystic kidney disease.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 300 papers, 1 of them a synthesis that pooled it.
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Who cites it
300 citing papers in PubMed, 1 synthesis or guideline pooled it, 582 citations in OpenAlex.
- Skin depletion of Kif3a resembles the pediatric atopic dermatitis transcriptome profile.Human molecular genetics · 2022Pooled it
- Cilia-to-basement membrane signaling is a biomechanical driver in models of autosomal dominant polycystic kidney disease.The Journal of clinical investigation · 2026Article
- Evidence for a tubular basement membrane-cilia connection in autosomal dominant polycystic kidney disease pathogenesis.The Journal of clinical investigation · 2026Article
- Structure Makes a Difference: IFT Complex in Ciliary Function and Ciliopathy.Cytoskeleton (Hoboken, N.J.) · 2026Review
- Structural basis of lipid-dependent allosteric gating mechanisms for PC1-PC2 ion channel.Nature communications · 2026Article
- Article
- Altered ciliary morphology reduces mechanosensation in a cystic kidney model as indicated by a mathematical model.Scientific reports · 2026Article
- Inflammation and Cyst Expansion in Polycystic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2025Article
- Macrophage Accumulation and Cyst Expansion in Pkd2 , Ift88 , and Double Mutant Mouse Models.Journal of the American Society of Nephrology : JASN · 2025Article
- The Role of ARL13B in Mitochondrial Homeostasis in Cultured Human Corneal Endothelial Cells.Investigative ophthalmology & visual science · 2025Article
- Loss of primary cilia promotes EphA2-mediated endothelial-to-mesenchymal transition in the ovarian tumor microenvironment.Molecular oncology · 2025Article
- Review
- Physiologic mechanisms underlying polycystic kidney disease.Physiological reviews · 2025Review
- Cholangiocyte ciliary defects induce sustained epidermal growth factor receptor signaling.Hepatology (Baltimore, Md.) · 2025Article
- Pathogenic Pathways and Therapeutic Strategies in Autosomal Dominant Polycystic Kidney Disease (ADPKD).Journal of cellular signaling · 2025Article
- Involvement of kinesins in skeletal dysplasia: a review.American journal of physiology. Cell physiology · 2024Review
- Emerging mechanistic understanding of cilia function in cellular signalling.Nature reviews. Molecular cell biology · 2024Review
- Overexpression of SMYD3 Promotes Autosomal Dominant Polycystic Kidney Disease by Mediating Cell Proliferation and Genome Instability.Biomedicines · 2024Article
- The exocyst complex and intracellular vesicles mediate soluble protein trafficking to the primary cilium.Communications biology · 2024Article
- The Cyst Epithelium in Polycystic Kidney Disease Patients Displays Normal Apical-Basolateral Cell Polarity.International journal of molecular sciences · 2024Article
240 more citing papers are in PubMed but not listed here.
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7 authors at 3 institutions in 1 country.
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Abstract
Polycystic kidney disease (PKD) is the most common genetic cause of renal failure in humans. Several proteins that are encoded by genes associated with PKD have recently been identified in primary cilia in renal tubular epithelia. These findings have suggested that abnormalities in cilia formation and function may play a role in the pathogenesis of PKD. To directly determine whether cilia are essential to maintain tubular integrity, we conditionally inactivated KIF3A, a subunit of kinesin-II that is essential for cilia formation, in renal epithelia. Constitutive inactivation of KIF3A produces abnormalities of left-right axis determination and embryonic lethality. Here we show that tissue-specific inactivation of KIF3A in renal tubular epithelial cells results in viable offspring with normal-appearing kidneys at birth. Cysts begin to develop in the kidney at postnatal day 5 and cause renal failure by postnatal day 21. The cyst epithelial cells lack primary cilia and exhibit increased proliferation and apoptosis, apical mislocalization of the epidermal growth factor receptor, increased expression of beta-catenin and c-Myc, and inhibition of p21(CIP1). These results demonstrate that the absence of renal cilia produces both the clinical and cell biological findings associated with PKD. Most generally, the phenotype of Kif3a mutant mice suggests a role for primary cilia in the maintenance of lumen-forming epithelial differentiation.
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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.