ArticleThe Journal of biological chemistry2010
TRPC3 regulates agonist-stimulated Ca2+ mobilization by mediating the interaction between type I inositol 1,4,5-trisphosphate receptor, RACK1, and Orai1.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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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
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.
- TRP Channels Interactome as a Novel Therapeutic Target in Breast Cancer.Frontiers in oncology · 2021Pooled it
- Neutrophil Mechanosignaling Promotes Integrin Engagement With Endothelial Cells and Motility Within Inflamed Vessels.Frontiers in immunology · 2018Trial
- 17β-Estradiol inhibits phosphorylation of stromal interaction molecule 1 (STIM1) protein: implication for store-operated calcium entry and chronic lung diseases.The Journal of biological chemistry · 2013Trial
- STIM-IP3R crosstalk regulates migration of breast cancer cells.The Journal of cell biology · 2025Article
- Agonist-Induced CaCells · 2024Article
- The T-type calcium channelosome.Pflugers Archiv : European journal of physiology · 2024Review
- Regulation of store-operated CaeLife · 2023Article
- Article
- A Comparative Perspective on Functionally-Related, Intracellular Calcium Channels: The Insect Ryanodine and Inositol 1,4,5-Trisphosphate Receptors.Biomolecules · 2021Review
- RACK1 plays a critical role in mast cell secretion and Ca2+ mobilization by modulating F-actin dynamics.Journal of cell science · 2021Article
- Proteins Interacting with STIM1 and Store-Operated CaProgress in molecular and subcellular biology · 2021Review
- Transient Receptor Potential Canonical (TRPC) Channels as Modulators of Migration and Invasion.International journal of molecular sciences · 2020Review
- Article
- Canonical Transient Receptor Potential Channels and Vascular Smooth Muscle Cell Plasticity.Journal of lipid and atherosclerosis · 2020Review
- CRAC channel regulation of innate immune cells in health and disease.Cell calcium · 2019Review
- Scaffold Proteins: From Coordinating Signaling Pathways to Metabolic Regulation.Endocrinology · 2018Review
- Association of the IP3R to STIM1 provides a reduced intraluminal calcium microenvironment, resulting in enhanced store-operated calcium entry.Scientific reports · 2018Article
- TRPC3 Channels in Cardiac Fibrosis.Frontiers in cardiovascular medicine · 2017Review
- Inositol 1,4,5-trisphosphate receptors and their protein partners as signalling hubs.The Journal of physiology · 2016Review
- Dynamic interaction of SARAF with STIM1 and Orai1 to modulate store-operated calcium entry.Scientific reports · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There is a body of evidence suggesting that Ca(2+) handling proteins assemble into signaling complexes required for a fine regulation of Ca(2+) signals, events that regulate a variety of critical cellular processes. Canonical transient receptor potential (TRPC) and Orai proteins have both been proposed to form Ca(2+)-permeable channels mediating Ca(2+) entry upon agonist stimulation. A number of studies have demonstrated that inositol 1,4,5-trisphosphate receptors (IP(3)Rs) interact with plasma membrane TRPC channels; however, at present there is no evidence supporting the interaction between Orai proteins and IP(3)Rs. Here we report that treatment with thapsigargin or cellular agonists results in association of Orai1 with types I and II IP(3)Rs. In addition, we have found that TRPC3, RACK1 (receptor for activated protein kinase C-1), and STIM1 (stromal interaction molecule 1) interact with Orai1 upon stimulation with agonists. TRPC3 expression silencing prevented both the interaction of Orai1 with TRPC3 and, more interestingly, the association of Orai1 with the type I IP(3)R, but not with the type II IP(3)R, thus suggesting that TRPC3 selectively mediates interaction between Orai1 and type I IP(3)R. In addition, TRPC3 expression silencing attenuated ATP- and CCh-stimulated interaction between RACK1 and the type I IP(3)R, as well as Ca(2+) release and entry. In conclusion, our results indicate that agonist stimulation results in the formation of an Orai1-STIM1-TRPC3-RACK1-type I IP(3)R complex, where TRPC3 plays a central role. This Ca(2+) signaling complex might be important for both agonist-induced Ca(2+) release and entry.
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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.