ArticlePloS one2019
The TRPP2-dependent channel of renal primary cilia also requires TRPM3.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Hyperosmolality activates polycystin-2 and TRPM4 in renal primary cilium.Pflugers Archiv : European journal of physiology · 2025Article
- Targeting TRPM3 as a potential therapeutic approach for autosomal dominant polycystic kidney disease.Scientific reports · 2025Article
- Genome-Based Advances in Modeling Renal Ciliopathies and Enhancing Patient Care.Kidney & blood pressure research · 2025Review
- Cardiovascular perspectives of the TRP channel polycystin 2.The Journal of physiology · 2024Article
- TRPM channels in health and disease.Nature reviews. Nephrology · 2024Review
- TRPP2 is located in the primary cilia of human non-pigmented ciliary epithelial cells.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2024Article
- Calcium signaling in polycystic kidney disease- cell death and survival.Cell calcium · 2023Review
- A plasma membrane-localized polycystin-1/polycystin-2 complex in endothelial cells elicits vasodilation.eLife · 2022Article
- Regenerative Calcium Currents in Renal Primary Cilia.Frontiers in physiology · 2022Article
- Inward CaAmerican journal of physiology. Renal physiology · 2021Article
- Distribution and Assembly of TRP Ion Channels.Advances in experimental medicine and biology · 2021Article
- TRPM3 in Brain (Patho)Physiology.Frontiers in cell and developmental biology · 2021Review
- Article
- Structure and function of polycystin channels in primary cilia.Cellular signalling · 2020Review
- Polycystins, ADPKD, and Cardiovascular Disease.Kidney international reports · 2020Review
- Lipid Interactions of a Ciliary Membrane TRP Channel: Simulation and Structural Studies of Polycystin-2.Structure (London, England : 1993) · 2020Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Primary cilia of renal epithelial cells express several members of the transient receptor potential (TRP) class of cation-conducting channel, including TRPC1, TRPM3, TRPM4, TRPP2, and TRPV4. Some cases of autosomal dominant polycystic kidney disease (ADPKD) are caused by defects in TRPP2 (also called polycystin-2, PC2, or PKD2). A large-conductance, TRPP2-dependent channel in renal cilia has been well described, but it is not known whether this channel includes any other protein subunits. To study this question, we investigated the pharmacology of the TRPP2-dependent channel through electrical recordings from the cilia of mIMCD-3 cells, a murine cell line of renal epithelial origin. The pharmacology was found to match that of TRPM3 channels. The ciliary TRPP2-dependent channel is known to be activated by depolarization and by increasing cytoplasmic Ca2+. This activation was greatly enhanced by external pregnenolone sulfate, an agonist of TRPM3 channels. Pregnenolone sulfate did not change the single-channel current-voltage relation. The channels were effectively blocked by isosakuranetin, a specific inhibitor of TRPM3 channels. Both pregnenolone sulfate and isosakuranetin were effective at concentrations as low as 1 μM. Knocking out TRPM3 by CRISPR/Cas9 genome editing eliminated the ciliary channel. Thus the channel is both TRPM3-dependent and TRPP2-dependent, suggesting that it may include both types of subunit. Knocking out TRPM3 did not change the level of TRPP2 protein in the cilia, so it is unlikely that the absence of functional ciliary channels results from a failure of 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.