ArticleThe EMBO journal1997
Minimal requirements for calcium oscillations driven by the IP3 receptor.
Article in The EMBO journal, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 182 citations in OpenAlex.
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- A tripartite organelle platform links growth factor receptor signaling to mitochondrial metabolism.Nature communications · 2024Article
- Cross Talking Calcium, IPCell biochemistry and biophysics · 2024Article
- ZneLife · 2023Article
- ZnbioRxiv : the preprint server for biology · 2023Article
- Structural titration reveals CaNature communications · 2023Article
- PKC Inhibits Sec61 Translocon-Mediated Sarcoplasmic Reticulum CaFrontiers in physiology · 2022Article
- Receptor-specific CaiScience · 2021Article
- A mathematical model of calcium dynamics: Obesity and mitochondria-associated ER membranes.PLoS computational biology · 2019Article
- Structural basis for the regulation of inositol trisphosphate receptors by CaNature structural & molecular biology · 2018Article
- Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles.Comprehensive Physiology · 2017Review
- Review
- Phosphatidylethanolamine Metabolism in Health and Disease.International review of cell and molecular biology · 2016Review
- The Phase Lag between Agonist-Induced Oscillatory CaCalcium signaling (Santa Clara, Calif.) · 2015Article
- Differential Regulation of Multiple Steps in Inositol 1,4,5-Trisphosphate Signaling by Protein Kinase C Shapes Hormone-stimulated Ca2+ Oscillations.The Journal of biological chemistry · 2015Article
- Rac-mediated Stimulation of Phospholipase Cγ2 Amplifies B Cell Receptor-induced Calcium Signaling.The Journal of biological chemistry · 2015Article
- Hormone-induced calcium oscillations depend on cross-coupling with inositol 1,4,5-trisphosphate oscillations.Cell reports · 2014Article
- Activation of Cdc42 is necessary for sustained oscillations of Ca2+ and PIP2 stimulated by antigen in RBL mast cells.Biology open · 2014Article
- Isoform- and species-specific control of inositol 1,4,5-trisphosphate (IP3) receptors by reactive oxygen species.The Journal of biological chemistry · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Hormones and neurotransmitters that act through inositol 1,4,5-trisphosphate (IP3) can induce oscillations of cytosolic Ca2+ ([Ca2+]c), which render dynamic regulation of intracellular targets. Imaging of fluorescent Ca2+ indicators located within intracellular Ca2+ stores was used to monitor IP3 receptor channel (IP3R) function and to demonstrate that IP3-dependent oscillations of Ca2+ release and re-uptake can be reproduced in single permeabilized hepatocytes. This system was used to define the minimum essential components of the oscillation mechanism. With IP3 clamped at a submaximal concentration, coordinated cycles of IP3R activation and subsequent inactivation were observed in each cell. Cycling between these states was dependent on feedback effects of released Ca2+ and the ensuing [Ca2+]c increase, but did not require Ca2+ re-accumulation. [Ca2+]c can act at distinct stimulatory and inhibitory sites on the IP3R, but whereas the Ca2+ release phase was driven by a Ca2+-induced increase in IP3 sensitivity, Ca2+ release could be terminated by intrinsic inactivation after IP3 bound to the Ca2+-sensitized IP3R without occupation of the inhibitory Ca2+-binding site. These findings were confirmed using Sr2+, which only interacts with the stimulatory site. Moreover, vasopressin induced Sr2+ oscillations in intact cells in which intracellular Ca2+ was completely replaced with Sr2+. Thus, [Ca2+]c oscillations can be driven by a coupled process of Ca2+-induced activation and obligatory intrinsic inactivation of the Ca2+-sensitized state of the IP3R, without a requirement for occupation of the inhibitory Ca2+-binding site.
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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.