ReviewCellular signalling2020
Polycystins as components of large multiprotein complexes of polycystin interactors.
Review in Cellular signalling, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Therapeutic Potential of Ketogenic Interventions for Autosomal-Dominant Polycystic Kidney Disease: A Systematic Review.Nutrients · 2024Pooled it
- The nonexcitable smooth muscle: remodeling the smooth muscle ion transport toolkit in disease.Physiological reviews · 2026Review
- Polycystin-1 and Cardiac Remodeling: From Mechanotransduction to Clinical Consequences.Circulation research · 2026Review
- Physiologic mechanisms underlying polycystic kidney disease.Physiological reviews · 2025Review
- Polycystins Expression in Astrocytic Gliomas.Biomedicines · 2025Article
- Vascular polycystin proteins in health and disease.Microcirculation (New York, N.Y. : 1994) · 2024Review
- Calcium channels as therapeutic targets in head and neck squamous cell carcinoma: current evidence and clinical trials.Frontiers in oncology · 2024Review
- CFTR and PC2, partners in the primary cilia in autosomal dominant polycystic kidney disease.American journal of physiology. Cell physiology · 2023Article
- Novel α-1,3-Glucosyltransferase Variants and Their Broad Clinical Polycystic Liver Disease Spectrum.Genes · 2023Article
- Hypoxia induces polycystin-1 expression in the renal epithelium.Royal Society open science · 2023Article
- Should we screen for intracranial aneurysms in children with autosomal dominant polycystic kidney disease?Pediatric nephrology (Berlin, Germany) · 2023Article
- Susceptibility genes of hyperuricemia and gout.Hereditas · 2022Review
- A plasma membrane-localized polycystin-1/polycystin-2 complex in endothelial cells elicits vasodilation.eLife · 2022Article
- Fission yeast polycystin Pkd2p promotes cell size expansion and antagonizes the Hippo-related SIN pathway.Journal of cell science · 2022Article
- Novel method for the genomic analysis ofFrontiers in cell and developmental biology · 2022Article
- The GPCR properties of polycystin-1- A new paradigm.Frontiers in molecular biosciences · 2022Review
- Cilia-Localized Counterregulatory Signals as Drivers of Renal Cystogenesis.Frontiers in molecular biosciences · 2022Review
- NMPA-approved traditional Chinese medicine-Pingwei Pill: new indication for colistin recovery against MCR-positive bacteria infection.Chinese medicine · 2021Article
- TRP channels in health and disease at a glance.Journal of cell science · 2021Article
- Comprehensive strategy improves the genetic diagnosis of different polycystic kidney diseases.Journal of cellular and molecular medicine · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Naturally occurring mutations in two separate genes, PKD1 and PKD2, are responsible for the vast majority of all cases of autosomal dominant polycystic kidney disease (ADPKD), one of the most common genetic diseases affecting 1 in 1000 Americans. The hallmark of ADPKD is the development of epithelial cysts in the kidney, liver, and pancreas. PKD1 encodes a large plasma membrane protein (PKD1, PC1, or Polycystin-1) with a long extracellular domain and has been speculated to function as an atypical G protein coupled receptor. PKD2 encodes an ion channel of the Transient Receptor Potential superfamily (TRPP2, PKD2, PC2, or Polycystin-2). Despite the identification of these genes more than 20 years ago, the molecular function of their encoded proteins and the mechanism(s) by which mutations in PKD1 and PKD2 cause ADPKD remain elusive. Genetic, biochemical, and functional evidence suggests they form a multiprotein complex present in multiple locations in the cell, including the plasma membrane, endoplasmic reticulum, and the primary cilium. Over the years, numerous interacting proteins have been identified using directed and unbiased approaches, and shown to modulate function, cellular localization, and protein stability and turnover of Polycystins. Delineation of the molecular composition of the Polycystin complex can have a significant impact on understanding their cellular function in health and disease states and on the identification of more specific and effective therapeutic targets.
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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.