ArticleMolecular biology of the cell2004
A polycystin-1 multiprotein complex is disrupted in polycystic kidney disease cells.
Article in Molecular biology of the cell, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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Who cites it
69 citing papers in PubMed, 142 citations in OpenAlex.
- Physiologic mechanisms underlying polycystic kidney disease.Physiological reviews · 2025Review
- Intestinal barrier function declines during polycystic kidney disease progression.American journal of physiology. Renal physiology · 2025Article
- Eliosin-an alternative product from the HmPKD1 locus is a component of endoplasmic reticulum mitochondria membrane contact sites.PloS one · 2025Article
- Cross-Species Insights into Autosomal Dominant Polycystic Kidney Disease: Provide an Alternative View on Research Advancement.International journal of molecular sciences · 2024Review
- Novel Potential Therapeutic Targets in Autosomal Dominant Polycystic Kidney Disease from the Perspective of Cell Polarity and Fibrosis.Biomolecules & therapeutics · 2024Review
- Polycystin-2 Mediated Calcium Signalling in theCells · 2024Article
- Role of ciliopathy protein TMEM107 in eye development: insights from a mouse model and retinal organoid.Life science alliance · 2023Article
- Autosomal Dominant Polycystic Kidney Disease: Is There a Role for Autophagy?International journal of molecular sciences · 2023Review
- Transient Receptor Potential Channels in the Epithelial-to-Mesenchymal Transition.International journal of molecular sciences · 2021Review
- Identification of pathological transcription in autosomal dominant polycystic kidney disease epithelia.Scientific reports · 2021Article
- Development of Glycerol-Rose Bengal-Polidocanol (GRP) foam for enhanced sclerosis of a cyst for cystic diseases.PloS one · 2021Article
- Urinary exosome proteomic profiling defines stage-specific rapid progression of autosomal dominant polycystic kidney disease and tolvaptan efficacy.BBA advances · 2021Article
- Polycystins as components of large multiprotein complexes of polycystin interactors.Cellular signalling · 2020Review
- GDNF drives rapid tubule morphogenesis in a novel 3DJournal of cell science · 2020Article
- Protein phosphatase 1α interacts with a novel ciliary targeting sequence of polycystin-1 and regulates polycystin-1 trafficking.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Autosomal dominant polycystic kidney disease: Disrupted pathways and potential therapeutic interventions.Journal of cellular physiology · 2019Review
- Synchronizing Protein Traffic to the Primary Cilium.Frontiers in genetics · 2019Article
- Polycystin and calcium signaling in cell death and survival.Cell calcium · 2018Review
- Ouabain promotes partial epithelial to mesenchymal transition (EMT) changes in human autosomal dominant polycystic kidney disease (ADPKD) cells.Experimental cell research · 2017Article
- Transcriptome analysis reveals manifold mechanisms of cyst development in ADPKD.Human genomics · 2016Article
9 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Autosomal dominant polycystic kidney disease (ADPKD) is typified by the accumulation of fluid-filled cysts and abnormalities in renal epithelial cell function. The disease is principally caused by mutations in the gene encoding polycystin-1, a large basolateral plasma membrane protein expressed in kidney epithelial cells. Our studies reveal that, in normal kidney cells, polycystin-1 forms a complex with the adherens junction protein E-cadherin and its associated catenins, suggesting a role in cell adhesion or polarity. In primary cells from ADPKD patients, the polycystin-1/polycystin-2/E-cadherin/beta-catenin complex was disrupted and both polycystin-1 and E-cadherin were depleted from the plasma membrane as a result of the increased phosphorylation of polycystin-1. The loss of E-cadherin was compensated by the transcriptional upregulation of the normally mesenchymal N-cadherin. Increased cell surface N-cadherin in the disease cells in turn stabilized the continued plasma membrane localization of beta-catenin in the absence of E-cadherin. The results suggest that enhanced phosphorylation of polycystin-1 in ADPKD cells precipitates changes in its localization and its ability to form protein complexes that are critical for the stabilization of adherens junctions and the maintenance of a fully differentiated polarized renal epithelium.
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Registered trials
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