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Cited by 2,575Ion Channels and ReceptorsCalcium signaling and nucleotide metabolismIon channel regulation and function

A model for receptor-regulated calcium entry

Putney, James W.·1986·Cell Calcium
DOI 10.1016/0143-4160(86)90026-6
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Abstract

A model is proposed for the mechanism by which activation of surface membrane receptors causes sustained Ca2+ entry into cells from the extracellular space. Reassessment of previously published findings on the behavior of receptor-regulated intracellular Ca2+ pools leads to the conclusion that when such pools are empty, a pathway from the extracellular space to the pool is opened; conversely when the pool is filled, the pathway is closed and it becomes relatively stable to depletion by low Ca2+ media or chelating agents. The biphasic nature of agonist-activated Ca2+-mobilization is thus seen as an initial emptying of the intracellular Ca2+ pool by inositol (1,4,5) trisphosphate, followed by rapid entry of Ca2+ into the pool and, in the continued presence of inositol (1,4,5) trisphosphate, into the cytosol. On withdrawal of agonist, inositol (1,4,5) trisphosphate is then rapidly degraded, the pathway from the pool to the cytosol is closed, and rapid entry from the outside continues until the Ca2+ content of the pool reaches a level that inactivates Ca2+ entry. This capacitative model allows for Ca2+ release and Ca2+ entry to be controlled by a single messenger, inositol (1,4,5) trisphosphate.

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Crossref · 10.1016/0143-4160(86)90026-6

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  • In eukaryotes, the ER constitutes a finite reservoir of Ca2+ primarily mobilized for signaling that must be replenished to sustain signaling and restore Ca2+ homeostasis.

    “It is known that in eukaryotes the ER constitutes a finite reservoir of Ca 2ϩ primarily mobilized for signaling that must be replenished to sustain the duration of signaling and ultimately restore Ca 2ϩ homeostasis in the ER and the cytosol (1-3, 32).”

    From Cch1 Restores Intracellular Ca2+ in Fungal Cells during Endoplasmic Reticulum Stress (2010) · cites this paper as [1]

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Authors
Putney, J. W.
Affiliations
Virginia Commonwealth University (US)
Corresponding author
Putney, James W.
ORCID
Putney, James W.
Venue
Cell Calcium
Publisher
Elsevier BV
Published
1986-02
Volume
7
Issue
1
Pages
1-12
ISSN
0143-4160 (ISSN-L)
DOI
10.1016/0143-4160(86)90026-6
OpenAlex
W2070832223
Cited by
2,575
References
35
Citations by year
2026: 26 · 2025: 29 · 2024: 36 · 2023: 37 · 2022: 44 · 2021: 56 · 2020: 53 · 2019: 48 · 2018: 59 · 2017: 83 · 2016: 74 · 2015: 52 · 2014: 57 · 2013: 83 · 2012: 85
FWCI
53.87
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Cell Calcium (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r01am032823-02)
  • National Institute of Dental and Craniofacial Research (DE-05764)
Topics
  • Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
Keywords
store-operated calcium entry, inositol trisphosphate, intracellular calcium stores, calcium mobilization, calcium release, calcium signaling, receptor activation
MeSH terms
Animals, Calcium, Cell Membrane, Hydrolysis, Inositol Phosphates, Ion Channels, Models, Biological, Phosphatidic Acids, Receptors, Cell Surface, Inositol 1,4,5-Trisphosphate, Lipid Metabolism

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