Evidence map›Paper›PMID 18036509›Full record

ArticleBiochemical pharmacology2008

Regulation of cyclic AMP response-element binding-protein (CREB) by Gq/11-protein-coupled receptors in human SH-SY5Y neuroblastoma cells.

Elizabeth M Rosethorne, Stefan R Nahorski, R A John Challiss

Open access · hybridAbstract read
In one paragraph

Article in Biochemical pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

18 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Genomic crosstalk between carbachol, a muscarinic receptor agonist, and the long-acting βThe Journal of pharmacology and experimental therapeutics · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. The M3-muscarinic receptor regulates learning and memory in a receptor phosphorylation/arrestin-dependent manner.Proceedings of the National Academy of Sciences of the United States of America · 2010
    Article
  15. CREB downregulation in vascular disease: a common response to cardiovascular risk.Arteriosclerosis, thrombosis, and vascular biology · 2010
    Article
  16. Article
  17. Article
  18. Article
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

3 authors at 1 institution in 1 country.

Elizabeth M RosethorneDepartment of Cell Physiology and Pharmacology, University of Leicester, Henry Wellcome Building, Lancaster Road, Leicester LE1 9HN, UK.
Stefan R Nahorski
R A John Challiss
University of Leicester · GB

Funding

Medical Research CouncilWellcome Trust 062495
6 · The paper itself

Abstract

Human SH-SY5Y neuroblastoma cells have been used to investigate mechanisms involved in CREB phosphorylation after activation of two endogenously expressed Gq/11-protein-coupled receptors, the M3 muscarinic acetylcholine (mACh) and B2 bradykinin receptors. Stimulation with either methacholine or bradykinin resulted in maximal increases in CREB phosphorylation within 1 min, with either a rapid subsequent decrease (bradykinin) to basal levels, or a sustained response (methacholine). Inhibitor studies were performed to assess the involvement of a number of potential kinases in signalling to CREB phosphorylation. Removal of extracellular Ca2+, inhibition of Ca2+/calmodulin-dependent protein kinase II and down-regulation of protein kinase C (PKC) resulted in reduced CREB phosphorylation after both M3 mACh and B2 bradykinin receptor activation. In contrast, inhibition of MEK1/2 by U0126 resulted in significantly reduced CREB phosphorylation levels after B2 bradykinin, but not M3 mACh receptor activation. In addition, we demonstrate that maintained phosphorylation of CREB is necessary for CRE-dependent gene transcription as the M3 mACh, but not the B2 bradykinin receptor activates both a recombinant CRE-dependent reporter gene, and the endogenous c-Fos gene. These data highlight the involvement of multiple, overlapping signalling pathways linking these endogenous Gq/11-coupled metabotropic receptors to CREB and emphasize the importance of the duration of signalling pathway activation in converting a CREB phosphorylation event into a significant change in transcriptional activity.

Indexed as

BradykininCalciumCell Line, TumorCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinExtracellular Signal-Regulated MAP KinasesGene Expression RegulationGTP-Binding Protein alpha Subunits, Gq-G11HumansMethacholine ChlorideNeuroblastomaPhosphatidylinositol 3-KinasesPhosphorylationProtein Kinase CReceptor, Bradykinin B2Receptors, G-Protein-CoupledBradykininCalciumCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinExtracellular Signal-Regulated MAP KinasesGTP-Binding Protein alpha Subunits, Gq-G11Methacholine ChloridePhosphatidylinositol 3-KinasesProtein Kinase CReceptor, Bradykinin B2Receptors, G-Protein-Coupled

Identifiers

PMID18036509
PMCPMC2593902
OpenAlexW1982718794

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.