ArticleThe Journal of general physiology2013
Quantitative properties and receptor reserve of the IP(3) and calcium branch of G(q)-coupled receptor signaling.
Article in The Journal of general physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 126 citations in OpenAlex.
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- Brain Capillary Ion Channels: Physiology and Channelopathies.Physiology (Bethesda, Md.) · 2026Review
- PIPProceedings of the National Academy of Sciences of the United States of America · 2025Article
- A computational framework for the investigation of phosphoinositide regulation.PLoS computational biology · 2025Article
- Biased signalingActa pharmaceutica Sinica. B · 2025Review
- Hippocampal Inhibitory Interneuron-Specific DREADDs Treatment Alters mTORC1-4E-BP Signaling and Impairs Memory Formation.Journal of neurochemistry · 2025Article
- Identification of secretory protein related biomarkers for primary biliary cholangitis based on machine learning and experimental validation.Open life sciences · 2025Article
- Neuroprotection against beta-amyloid toxicity by the novel estrogen receptor modulator STX requires convergent signaling pathways.Frontiers in molecular neuroscience · 2025Article
- Insights on Platelet-Derived Growth Factor Receptor α-Positive Interstitial Cells in the Male Reproductive Tract.International journal of molecular sciences · 2024Review
- α-Synuclein-dependent increases in PIP5K1γ drive inositol signaling to promote neurotoxicity.Cell reports · 2023Article
- Contribution of TRPC3-mediated CaPflugers Archiv : European journal of physiology · 2023Article
- Involvement of CaCellular and molecular neurobiology · 2023Article
- Insulin: A connection between pancreatic β cells and the hypothalamus.World journal of diabetes · 2023Review
- Postsynaptic Proteins at Excitatory Synapses in the Brain-Relationship with Depressive Disorders.International journal of molecular sciences · 2022Review
- Biophysical physiology of phosphoinositide rapid dynamics and regulation in living cells.The Journal of general physiology · 2022Article
- Hippocampal neurons maintain a large PtdIns(4)P pool that results in faster PtdIns(4,5)P2 synthesis.The Journal of general physiology · 2022Article
- PIPCommunications biology · 2022Article
- Engaging biological oscillators through second messenger pathways permits emergence of a robust gastric slow-wave during peristalsis.PLoS computational biology · 2021Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
Gq-coupled plasma membrane receptors activate phospholipase C (PLC), which hydrolyzes membrane phosphatidylinositol 4,5-bisphosphate (PIP2) into the second messengers inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). This leads to calcium release, protein kinase C (PKC) activation, and sometimes PIP2 depletion. To understand mechanisms governing these diverging signals and to determine which of these signals is responsible for the inhibition of KCNQ2/3 (KV7.2/7.3) potassium channels, we monitored levels of PIP2, IP3, and calcium in single living cells. DAG and PKC are monitored in our companion paper (Falkenburger et al. 2013. J. Gen. Physiol. http://dx.doi.org/10.1085/jgp.201210887). The results extend our previous kinetic model of Gq-coupled receptor signaling to IP3 and calcium. We find that activation of low-abundance endogenous P2Y2 receptors by a saturating concentration of uridine 5'-triphosphate (UTP; 100 µM) leads to calcium release but not to PIP2 depletion. Activation of overexpressed M1 muscarinic receptors by 10 µM Oxo-M leads to a similar calcium release but also depletes PIP2. KCNQ2/3 channels are inhibited by Oxo-M (by 85%), but not by UTP (<1%). These differences can be attributed purely to differences in receptor abundance. Full amplitude calcium responses can be elicited even after PIP2 was partially depleted by overexpressed inducible phosphatidylinositol 5-phosphatases, suggesting that very low amounts of IP3 suffice to elicit a full calcium release. Hence, weak PLC activation can elicit robust calcium signals without net PIP2 depletion or KCNQ2/3 channel inhibition.
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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.