ArticleCellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology2011
Polycystin-1, 2, and STIM1 interact with IP(3)R to modulate ER Ca release through the PI3K/Akt pathway.
Article in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 77 citations in OpenAlex.
- The Ion channel, CFTR, assembles with HIPPO pathway proteins TAZ and YAP in polycystic kidney disease.The Journal of biological chemistry · 2026Article
- Review
- Review
- Regulation of store-operated CaeLife · 2023Article
- Polycystin Channel Complexes.Annual review of physiology · 2023Review
- Plant-derived compounds for treating autosomal dominant polycystic kidney disease.Frontiers in nephrology · 2023Review
- Chlamydia trachomatis suppresses host cell store-operated CaScientific reports · 2022Article
- Autosomal Dominant Polycystic Kidney Disease: From Pathophysiology of Cystogenesis to Advances in the Treatment.International journal of molecular sciences · 2022Review
- Implications of Phosphoinositide 3-Kinase-Akt (PI3K-Akt) Pathway in the Pathogenesis of Alzheimer's Disease.Molecular neurobiology · 2022Review
- Role of PKD2 in the endoplasmic reticulum calcium homeostasis.Frontiers in physiology · 2022Review
- VAP Proteins - From Organelle Tethers to Pathogenic Host Interactors and Their Role in Neuronal Disease.Frontiers in cell and developmental biology · 2022Review
- The Mitochondrial CaCell calcium · 2022Article
- Endoplasmic Reticulum Calcium Homeostasis in Kidney Disease: Pathogenesis and Therapeutic Targets.The American journal of pathology · 2021Review
- More Than Just Simple Interaction between STIM and Orai Proteins: CRAC Channel Function Enabled by a Network of Interactions with Regulatory Proteins.International journal of molecular sciences · 2021Review
- Insights Into the Molecular Mechanisms of Polycystic Kidney Diseases.Frontiers in physiology · 2021Review
- Proteins Interacting with STIM1 and Store-Operated CaProgress in molecular and subcellular biology · 2021Review
- Disrupting polycystin-2 EF hand CaJournal of cell science · 2020Article
- TRPP2 and STIM1 form a microdomain to regulate store-operated CaCell communication and signaling : CCS · 2020Article
- Modulation of polycystic kidney disease by G-protein coupled receptors and cyclic AMP signaling.Cellular signalling · 2020Review
- Polycystin 2: A calcium channel, channel partner, and regulator of calcium homeostasis in ADPKD.Cellular signalling · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Dysregulation of Ca(2+) signaling and homeostasis has been linked to the development of ADPKD through aberrant functioning of the polycystins. In this study, we investigated the role of the polycystins in modulating Ca(2+) signaling. Expression of full-length PC1 in MDCK cells inhibited intracellular Ca(2+) release in response to ATP when compared to control cells. This phenotype correlated with reduced interaction of endogenous PC2 and IP(3)R in PC1-containing cells. We also found that endogenous STIM1 also interacted with the IP(3)R, and this interaction was enhanced by PC1 expression. Increased interaction between STIM1 and IP(3)R inhibited Ca(2+) release. PC1 regulates intracellular Ca(2+) release and the interaction of PC2-IP(3)R-STIM1 through the PI3K/Akt signaling pathway. Inhibition of the PI3K/Akt pathway in PC1 containing cells restored intracellular Ca(2+) release, increased the interaction between PC2 and IP(3)R and disrupted the STIM1-IP(3)R complex. Conversely, activation of the PI3K/Akt signaling pathway by HGF in control MDCK cells gave the reverse effects. It reduced the release of Ca(2+) to levels comparable to the PC1 cells, inhibited the association PC2 and IP(3)R, and increased the interaction between STIM and IP(3)R. Overall, our studies provide a potential mechanism for the modulation of intracellular Ca(2+) signaling by the polycystins.
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.