ArticleThe Journal of cell biology2000
Compromised cytoarchitecture and polarized trafficking in autosomal dominant polycystic kidney disease cells.
Article in The Journal of cell biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 128 citations in OpenAlex.
- Inverted apicobasal polarity in health and disease.Journal of cell science · 2024Review
- CFTR and PC2, partners in the primary cilia in autosomal dominant polycystic kidney disease.American journal of physiology. Cell physiology · 2023Article
- Polycystin-1 Interacting Protein-1 (CU062) Interacts with the Ectodomain of Polycystin-1 (PC1).Cells · 2023Article
- Glucose absorption drives cystogenesis in a human organoid-on-chip model of polycystic kidney disease.Nature communications · 2022Article
- Proliferative signaling by ERBB proteins and RAF/MEK/ERK effectors in polycystic kidney disease.Cellular signalling · 2020Review
- Pharmacological reversal of renal cysts from secretion to absorption suggests a potential therapeutic strategy for managing autosomal dominant polycystic kidney disease.The Journal of biological chemistry · 2019Article
- Fundamental insights into autosomal dominant polycystic kidney disease from human-based cell models.Pediatric nephrology (Berlin, Germany) · 2019Article
- The association between autosomal dominant polycystic kidney disease and cancer.International urology and nephrology · 2019Review
- Regulation of Cell Polarity by Exocyst-Mediated Trafficking.Cold Spring Harbor perspectives in biology · 2018Review
- Ouabain promotes partial epithelial to mesenchymal transition (EMT) changes in human autosomal dominant polycystic kidney disease (ADPKD) cells.Experimental cell research · 2017Article
- On the Many Actions of Ouabain: Pro-Cystogenic Effects in Autosomal Dominant Polycystic Kidney Disease.Molecules (Basel, Switzerland) · 2017Review
- A holey pursuit: lumen formation in the developing kidney.Pediatric nephrology (Berlin, Germany) · 2017Review
- Virtual-tissue computer simulations define the roles of cell adhesion and proliferation in the onset of kidney cystic disease.Molecular biology of the cell · 2016Article
- A polycystin-centric view of cyst formation and disease: the polycystins revisited.Kidney international · 2015Review
- The hallmarks of cancer: relevance to the pathogenesis of polycystic kidney disease.Nature reviews. Nephrology · 2015Review
- Modulation of the secretory pathway rescues zebrafish polycystic kidney disease pathology.Journal of the American Society of Nephrology : JASN · 2014Article
- Cell polarity and cystic kidney disease.Pediatric nephrology (Berlin, Germany) · 2013Review
- A telomerase immortalized human proximal tubule cell line with a truncation mutation (Q4004X) in polycystin-1.PloS one · 2013Article
- c-Met and NF-κB-dependent overexpression of Wnt7a and -7b and Pax2 promotes cystogenesis in polycystic kidney disease.Journal of the American Society of Nephrology : JASN · 2012Article
- Receptor protein tyrosine phosphatases are novel components of a polycystin complex.Biochimica et biophysica acta · 2011Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Cystogenesis associated with autosomal dominant polycystic kidney disease (ADPKD) is characterized by perturbations in the polarized phenotype and function of cyst-lining epithelial cells. The polycystins, the protein products of the genes mutated in the majority of ADPKD cases, have been described recently, but the pathological mechanism by which causal mutations result in the mislocalization of cell membrane proteins has remained unclear. This report documents the dissociation from the ADPKD cell basolateral membrane of three molecules essential for spatial organization and exocytosis. The adherens junction protein E-cadherin, the subcellular disposition of which governs intercellular and intracellular architecture, was discovered sequestered in an internal ADPKD cell compartment. At the same time, sec6 and sec8, components of a complex critical for basolateral cargo delivery normally arrayed at the apico-lateral apex, were depleted from the ADPKD cell plasma membrane. An analysis of membrane transport revealed that basolateral trafficking of proteins and lipids was impaired as a result of delayed cargo exit from the ADPKD cell Golgi apparatus. Apical transport proceeded normally. Taken together with recent documentation of an association between polycystin-1 and E-cadherin (Huan and van Adelsberg 1999), the data suggest that causal mutations disrupt E-cadherin-dependent cytoarchitecture, adversely affecting protein assemblies crucial for basolateral trafficking.
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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.