ArticleThe Biochemical journal2001
Control of Ca2+ influx in human neutrophils by inositol 1,4,5-trisphosphate (IP3) binding: differential effects of micro-injected IP3 receptor antagonists.
Article in The Biochemical journal, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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
6 citing papers in PubMed, 27 citations in OpenAlex.
- Fucoidan inhibits Ca2+ responses induced by a wide spectrum of agonists for G‑protein‑coupled receptors.Molecular medicine reports · 2018Article
- Ca²⁺ and calpain control membrane expansion during the rapid cell spreading of neutrophils.Journal of cell science · 2013Article
- Activation of the inositol (1,4,5)-triphosphate calcium gate receptor is required for HIV-1 Gag release.Journal of virology · 2010Article
- Taming the neutrophil: calcium clearance and influx mechanisms as novel targets for pharmacological control.Clinical and experimental immunology · 2005Review
- Article
- Ca2+ influx shutdown during neutrophil apoptosis: importance and possible mechanism.Immunology · 2004Review
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophils signal Ca2+ changes in response to occupancy of G-protein-linked receptors such as the formylated peptide receptor. This Ca2+ signal is composed of two parts, inositol 1,4,5-trisphosphate (IP3)-triggered release of Ca2+ from an intracellular store and Ca2+ influx. In order to probe the relationship between these events, cytosolic free Ca2+ changes in neutrophils were monitored after micro-injection of agents which inhibit IP3 binding. Micro-injection of heparin into neutrophils totally inhibited both formylmethionyl-leucylphenylalanine-induced Ca2+ release and the subsequent Ca2+ influx. This effect was not due to prior depletion of Ca2+ stores. Furthermore, micro-injection with anti-IP3-receptor antibody also inhibited Ca2+ release. However, anti-IP3-receptor antibody and another high-molecular-mass IP3-binding antagonist, heparin-albumin conjugate, failed to inhibit the accompanying Ca2+ influx. It was concluded that two IP3-binding sites exist in neutrophils: one accessible by both heparin and the high-molecular-mass inhibitors of IP3 binding and responsible for Ca2+ release, and another inaccessible to high-molecular-mass molecules and responsible for Ca2+ influx.
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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.