ArticleAmerican journal of physiology. Renal physiology2015
A TRPM4-dependent current in murine renal primary cilia.
Article in American journal of physiology. Renal physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 29 citations in OpenAlex.
- Abnormal purinergic signaling contributes to development of renal cysts in autosomal dominant polycystic kidney disease.Purinergic signalling · 2026Article
- Structural biology of the TRPM4 channel: architecture, modulation, and therapeutic opportunities.Frontiers in pharmacology · 2026Review
- Hyperosmolality activates polycystin-2 and TRPM4 in renal primary cilium.Pflugers Archiv : European journal of physiology · 2025Article
- Pharmacological Modulation and (Patho)Physiological Roles of TRPM4 Channel-Part 1: Modulation of TRPM4.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Regenerative Calcium Currents in Renal Primary Cilia.Frontiers in physiology · 2022Article
- Pharmacological Modulation and (Patho)Physiological Roles of TRPM4 Channel-Part 2: TRPM4 in Health and Disease.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Inward CaAmerican journal of physiology. Renal physiology · 2021Article
- Species-Specific Effects of Cation Channel TRPM4 Small-Molecule Inhibitors.Frontiers in pharmacology · 2021Article
- Doxycycline Changes the Transcriptome Profile of mIMCD3 Renal Epithelial Cells.Frontiers in physiology · 2021Article
- Article
- The Enigmatic Role of Lipids in Cilia Signaling.Frontiers in cell and developmental biology · 2020Review
- Article
- GLIS1-3 transcription factors: critical roles in the regulation of multiple physiological processes and diseases.Cellular and molecular life sciences : CMLS · 2018Review
- Progress in ciliary ion channel physiology.The Journal of general physiology · 2017Review
- The native TRPP2-dependent channel of murine renal primary cilia.American journal of physiology. Renal physiology · 2017Article
- Calcium channels in primary cilia.Current opinion in nephrology and hypertension · 2016Review
- Concurrent Gitelman Syndrome-like Tubulopathy and Grave's Disease.Indian journal of nephrologyArticle
Corrections and comments
- Commented on byBeing dedicated.2015
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Defects in primary cilia lead to a variety of human diseases. One of these, polycystic kidney disease, can be caused by defects in a Ca²⁺-gated ion channel (TRPP2) found on the cilium. Other ciliary functions also contribute to cystogenesis, and defects in apical Ca²⁺ homeostasis have been implicated. By recording directly from the native cilia of mIMCD-3 cells, a murine cell line of renal epithelial origin, we have identified a second Ca²⁺-gated channel in the ciliary membrane: the transient receptor potential cation channel, subfamily M, member 4 (TRPM4). In excised primary cilia, TRPM4 was found to have a low sensitivity to Ca²⁺, with an EC₅₀ of 646 μM at +100 mV. It was inhibited by MgATP and by 9-phenanthrol. The channel was not permeable to Ca²⁺ or Cl⁻ and had a permeability ratio PK/PNa of 1.42. Reducing the expression of Trpm4 mRNA with short hairpin (sh) RNA reduced the TRPM4 current by 87% and shortened primary cilia by 43%. When phospholipase C was inhibited, the sensitivity to cytoplasmic Ca²⁺ greatly increased (EC₅₀ = 26 μM at +100 mV), which is consistent with previous reports that phosphatidylinositol 4,5-bisphosphate (PIP2) modulates the channel. MgATP did not restore the channel to a preinactivation state, suggesting that the enzyme or substrate necessary for making PIP2 is not abundant in primary cilia of mIMCD-3 cells. The function of TRPM4 in renal primary cilia is not yet known, but it is likely to influence the apical Ca²⁺ dynamics of the cell, perhaps in tandem with TRPP2.
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.