ArticleBritish journal of pharmacology1992
Inositol 1,4,5-trisphosphate generation and calcium mobilisation via activation of an atypical P2 receptor in the neuronal cell line, N1E-115.
Article in British journal of pharmacology, 1992. 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.
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Who cites it
6 citing papers in PubMed, 18 citations in OpenAlex.
- Purinergic signalling and cancer.Purinergic signalling · 2013Review
- Actions of ADP, but not ATP, on cytosolic free Ca2+ in single rat hepatocytes mimicked by 2-methylthioATP.British journal of pharmacology · 1995Article
- Synergy between the inositol phosphate responses to transfected human adenosine A1-receptors and constitutive P2-purinoceptors in CHO-K1 cells.British journal of pharmacology · 1995Article
- Stimulation by extracellular ATP and UTP of the mitogen-activated protein kinase cascade and proliferation of rat renal mesangial cells.British journal of pharmacology · 1994Article
- Increases in intracellular calcium via activation of an endogenous P2-purinoceptor in cultured CHO-K1 cells.British journal of pharmacology · 1993Article
- Extracellular ATP and UTP activation of phospholipase D is mediated by protein kinase C-epsilon in rat renal mesangial cells.British journal of pharmacology · 1993Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
1. Alterations in the levels of intracellular calcium ([Ca2+]i) and D-myo-inositol-1,4,5-trisphosphate (InsP3) were measured in the murine neuroblastoma cell line clone, N1E-115, by use of the calcium-sensitive dye, fura-2 and a radioreceptor assay, respectively. 2. Exposure of the cells to ATP (100 microM) elicited rapid and transient increases in [Ca2+]i and InsP3, with both responses reaching a maximum between 10-20 s after agonist addition. 3. Investigation of concentration-response data by use of various analogues of ATP suggests the presence of an extracellular receptor which fails to fit into the current classification of purinoceptors. 4. Cross-desensitization experiments suggest that the same receptor can also be activated by the structurally different pyrimidine base, UTP. 5. Application of the tumour-promoting agent, beta-phorbol-12,13 dibutyrate (PDBu) caused a reduction in the increases in both [Ca2+]i and InsP3, suggesting a role for protein kinase C in feedback inhibition of purinoceptor responses in this cell line. 6. In summary, we present the first evidence for the existence of an atypical purinoceptor on a cell line of CNS origin. This receptor is linked to stimulation of phosphoinositide turnover and subsequent mobilisation of intracellular calcium.
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