ReviewCellular signalling2020
Polycystin 2: A calcium channel, channel partner, and regulator of calcium homeostasis in ADPKD.
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 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
28 citing papers in PubMed, 47 citations in OpenAlex.
- The nonexcitable smooth muscle: remodeling the smooth muscle ion transport toolkit in disease.Physiological reviews · 2026Review
- Primary cilia-extracellular vesicle crosstalk in Alzheimer's disease: Emerging mechanisms and biomarker potential.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- The Important Role of Polycystin in the Skeletal System.Calcified tissue international · 2026Review
- Functional Coupling of Calcium-Sensing Receptor and Polycystin-2 in Renal Epithelial Cells: Physiological Role and Potential Therapeutic Target in Polycystic Kidney Disease.International journal of molecular sciences · 2025Article
- Strategies for multimodal spatiotemporal profiling of phosphorylation in cilia biology.Journal of cell science · 2025Review
- Physiologic mechanisms underlying polycystic kidney disease.Physiological reviews · 2025Review
- Polycystins Expression in Astrocytic Gliomas.Biomedicines · 2025Article
- Review
- Hyperosmolality activates polycystin-2 and TRPM4 in renal primary cilium.Pflugers Archiv : European journal of physiology · 2025Article
- Breaking Left-Right Symmetry by the Interplay of Planar Cell Polarity, Calcium Signaling and Cilia.Cells · 2024Review
- Disease-associated missense mutations in the pore loop of polycystin-2 alter its ion channel function in a heterologous expression system.The Journal of biological chemistry · 2024Article
- Vascular polycystin proteins in health and disease.Microcirculation (New York, N.Y. : 1994) · 2024Review
- Clinical manifestation, epidemiology, genetic basis, potential molecular targets, and current treatment of polycystic liver disease.Orphanet journal of rare diseases · 2024Review
- Comparative analysis of SEC61A1 mutant R236C in two patient-derived cellular platforms.Scientific reports · 2024Article
- Polycystin-2 Mediated Calcium Signalling in theCells · 2024Article
- Novel α-1,3-Glucosyltransferase Variants and Their Broad Clinical Polycystic Liver Disease Spectrum.Genes · 2023Article
- Transcriptional Basis of CaCancers · 2023Article
- [Low-frequency pulsed electromagnetic fields promote osteoblast mineralization and maturation of rats through the PC2/sAC/PKA/CREB signaling pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- A plasma membrane-localized polycystin-1/polycystin-2 complex in endothelial cells elicits vasodilation.eLife · 2022Article
- Recent advances in understanding ion transport mechanisms in polycystic kidney disease.Clinical science (London, England : 1979) · 2021Review
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
Polycystin 2 (PC2) is one of two main protein types responsible for the underlying etiology of autosomal dominant polycystic kidney disease (ADPKD), the most prevalent monogenic renal disease in the world. This debilitating and currently incurable condition is caused by loss-of-function mutations in PKD2 and PKD1, the genes encoding for PC2 and Polycystin 1 (PC1), respectively. Two-hit mutation events in these genes lead to renal cyst formation and eventual kidney failure, the main hallmarks of ADPKD. Though much is known concerning the physiological consequences and dysfunctional signaling mechanisms resulting from ADPKD development, to best understand the requirement of PC2 in maintaining organ homeostasis, it is important to recognize how PC2 acts under normal conditions. As such, an array of work has been performed characterizing the endogenous function of PC2, revealing it to be a member of the transient receptor potential (TRP) channel family of proteins. As a TRP protein, PC2 is a nonselective, cation-permeant, calcium-sensitive channel expressed in all tissue types, where it localizes primarily on the endoplasmic reticulum (ER), primary cilia, and plasma membrane. In addition to its channel function, PC2 interacts with and acts as a regulator of a number of other channels, ultimately further affecting intracellular signaling and leading to dysfunction in its absence. In this review, we describe the biophysical and physiological properties of PC2 as a cation channel and modulator of intracellular calcium channels, along with how these properties are altered in ADPKD.
Indexed as
Identifiers
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.