ArticleJournal of cell science2009
Homophilic and heterophilic polycystin 1 interactions regulate E-cadherin recruitment and junction assembly in MDCK cells.
Article in Journal of cell science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 33 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 53 citations in OpenAlex.
- Deep learning-supported image quantification of epithelial cell shapes and its application to polycystic kidney disease.PLoS computational biology · 2026Article
- Physiologic mechanisms underlying polycystic kidney disease.Physiological reviews · 2025Review
- Mechanisms of Cyst Development in Polycystic Kidney Disease.Advances in kidney disease and health · 2023Review
- Article
- Polycystin-1 modulates RUNX2 activation and osteocalcin gene expression via ERK signalling in a human craniosynostosis cell model.Journal of cellular and molecular medicine · 2021Article
- Polycystin-1 regulates ARHGAP35-dependent centrosomal RhoA activation and ROCK signaling.JCI insight · 2020Article
- Adhesion GPCRs as a paradigm for understanding polycystin-1 G protein regulation.Cellular signalling · 2020Review
- STAT signaling in polycystic kidney disease.Cellular signalling · 2020Review
- Sensing of tubular flow and renal electrolyte transport.Nature reviews. Nephrology · 2020Review
- Polycystin-1 affects cancer cell behaviour and interacts with mTOR and Jak signalling pathways in cancer cell lines.Journal of cellular and molecular medicine · 2019Article
- Ouabain promotes partial epithelial to mesenchymal transition (EMT) changes in human autosomal dominant polycystic kidney disease (ADPKD) cells.Experimental cell research · 2017Article
- Mechanosensor polycystin-1 potentiates differentiation of human osteoblastic cells by upregulating Runx2 expression via induction of JAK2/STAT3 signaling axis.Cellular and molecular life sciences : CMLS · 2017Article
- A holey pursuit: lumen formation in the developing kidney.Pediatric nephrology (Berlin, Germany) · 2017Review
- Gα12 is required for renal cystogenesis induced by Pkd1 inactivation.Journal of cell science · 2016Article
- The Polycystin-1, Lipoxygenase, and α-Toxin Domain Regulates Polycystin-1 Trafficking.Journal of the American Society of Nephrology : JASN · 2016Article
- A polycystin-centric view of cyst formation and disease: the polycystins revisited.Kidney international · 2015Review
- Regulation of the microtubular cytoskeleton by Polycystin-1 favors focal adhesions turnover to modulate cell adhesion and migration.BMC cell biology · 2015Article
- Polycystins and partners: proposed role in mechanosensitivity.The Journal of physiology · 2014Review
- Polycystin-1 cleavage and the regulation of transcriptional pathways.Pediatric nephrology (Berlin, Germany) · 2014Review
- Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited human renal disease and is caused by mutations in two genes, PKD1 (85%) and PKD2 (15%). Cyst epithelial cells are characterised by a complex cellular phenotype including changes in proliferation, apoptosis, basement membrane composition and apicobasal polarity. Since polycystin 1 (PC1), the PKD1 protein, has been located in the basolateral membrane of kidney epithelial cells, we hypothesised that it might have a key role in mediating or stabilising cell-cell interactions. In non-ciliated L929 cells, stable or transient surface expression of the PC1 extracellular domain was sufficient to confer an adhesive phenotype and stimulate junction formation. In MDCK cells, we found that PC1 was recruited to the lateral membranes coincident with E-cadherin within 30 minutes after a ;calcium switch'. Recruitment of both proteins was significantly delayed when cells were treated with a PC1 blocking antibody raised to the PKD domains. Finally, PC1 and E-cadherin could be coimmunoprecipitated together from MDCK cells. We conclude that PC1 has a key role in initiating junction formation via initial homophilic interactions and facilitates junction assembly and the establishment of apicobasal polarity by E-cadherin recruitment.
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What OpenQuestion holds
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.