Evidence map›Paper›PMID 8526880›Full record

ArticleThe Biochemical journal1995

Activation of mitogen-activated protein kinases by stimulation of the central cannabinoid receptor CB1.

M Bouaboula, C Poinot-Chazel, B Bourrié, X Canat, B Calandra, M Rinaldi-Carmona, G Le Fur, P Casellas

Open access · bronzeAbstract read
In one paragraph

Article in The Biochemical journal, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 146 papers.

0numbers the graph read from it
0cells of the map it votes in
146citing papers in PubMed
10.5field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

146 citing papers in PubMed, 537 citations in OpenAlex.

  1. CNR1 and CNR2 Cannabinoid Receptor Mutations in Cancer Cells.Current issues in molecular biology · 2026
    Article
  2. Review
  3. Canonical Cannabinoid Receptors.Current topics in behavioral neurosciences · 2026
    Review
  4. Review
  5. Review
  6. Cannabinoids: Role in Neurological Diseases and Psychiatric Disorders.International journal of molecular sciences · 2024
    Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Mechanisms of cannabinoid tolerance.Biochemical pharmacology · 2023
    Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  19. Genes · 2021
    Review
  20. Review

86 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

M BouaboulaSanofi Recherche, Department of Immunopharmacology, Montpellier, France.
C Poinot-Chazel
B Bourrié
X Canat
B Calandra
M Rinaldi-Carmona
G Le Fur
P Casellas
Sanofi (France) · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The G-protein-coupled central cannabinoid receptor (CB1) has been shown to be functionally associated with several biological responses including inhibition of adenylate cyclase, modulation of ion channels and induction of the immediate-early gene Krox-24. Using stably transfected Chinese Hamster Ovary cells expressing human CB1 we show here that cannabinoid treatment induces both phosphorylation and activation of mitogen-activated protein (MAP) kinases, and that these effects are inhibited by SR 141716A, a selective CB1 antagonist. The two p42 and p44 kDa MAP kinases are activated in a time- and dose-dependent manner. The rank order of potency for the activation of MAP kinases with various cannabinoid agonists is CP-55940 > delta 9-tetrahydrocannabinol > WIN 55212.2, in agreement with the pharmacological profile of CB1. The activation of MAP kinases is blocked by pertussis toxin but not by treatment with hydrolysis-resistant cyclic AMP analogues. This suggests that the signal transduction pathway between CB1 and MAP kinases involves a pertussis-toxin-sensitive GTP-binding protein and is independent of cyclic AMP metabolism. This coupling of CB1 subtype and mitogenic signal pathway, also observed in the human astrocytoma cell line U373 MG, may explain the mechanism of action underlying cannabinoid-induced Krox-24 induction.

Indexed as

Immediate-Early Proteins1-Methyl-3-isobutylxanthine8-Bromo Cyclic Adenosine MonophosphateAdenylate Cyclase ToxinAnalgesicsAnimalsBenzoquinonesBucladesineCalcium-Calmodulin-Dependent Protein KinasesCannabinoidsCell LineCHO CellsCricetinaeCyclohexanolsDNA-Binding ProteinsEarly Growth Response Protein 11-Methyl-3-isobutylxanthine3-(2-hydroxy-4-(1,1-dimethylheptyl)phenyl)-4-(3-hydroxypropyl)cyclohexanol8-Bromo Cyclic Adenosine MonophosphateAdenylate Cyclase ToxinAnalgesicsBenzoquinonesBucladesineCalcium-Calmodulin-Dependent Protein KinasesCannabinoidsCyclohexanolsDNA-Binding ProteinsEarly Growth Response Protein 1EGR1 protein, humanEnzyme InhibitorsGTP-Binding ProteinsherbimycinImmediate-Early ProteinsLactams, MacrocyclicPertussis ToxinPiperidinesPyrazolesQuinonesReceptors, CannabinoidReceptors, DrugRecombinant ProteinsRifabutinRimonabantTetradecanoylphorbol AcetateTranscription FactorsVirulence Factors, Bordetella

Identifiers

PMID8526880
PMCPMC1136308
OpenAlexW1812356957

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.