Evidence map›Paper›PMID 9078236›Full record

ReviewThe Biochemical journal1997

Regulatory mechanisms that modulate signalling by G-protein-coupled receptors.

S K Böhm, E F Grady, N W Bunnett

Open access · bronzeAbstract readReview
In one paragraph

Review in The Biochemical journal, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
19.1field-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

78 citing papers in PubMed, 506 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Update of Gepants in the Treatment of Chronic Migraine.Current pain and headache reports · 2023
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Recovery sleep after extended wakefulness restores elevated AProceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  19. Review
  20. Article

18 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

3 authors at 1 institution in 1 country.

S K BöhmDepartment of Surgery, University of California, San Francisco 94143-0660, USA.
E F Grady
N W Bunnett
University of California, San Francisco · US

Funding

REGULATION OF CELLULAR RESPONSES TO NEUROPEPTIDESR37DK039957 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BUNNETT, NIGEL W · 2000 to 2010
$3.2M
NEURAL REGULATION OF PANCREATIC FUNCTIONR01DK046285 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KIRKWOOD, KIMBERLY SAUNDERS · 1994 to 2012
$2.1M
REGULATION OF CELLULAR RESPONSES TO NEUROPEPTIDESR01DK039957 · NIDDK · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI BUNNETT, NIGEL W · 1987 to 1998
–
MODULATION OF LYMPHOCYTE FUNCTION BY SUBSTANCE PR01NS021710 · NINDS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI PAYAN, DONALD G · 1985 to 1997
–
NIDDK NIH HHS DK 39957NIDDK NIH HHS DK 46285NINDS NIH HHS NS 21710
6 · The paper itself

Abstract

The large and functionally diverse group of G-protein-coupled receptors includes receptors for many different signalling molecules, including peptide and non-peptide hormones and neuro-transmitters, chemokines, prostanoids and proteinases. Their principal function is to transmit information about the extracellular environment to the interior of the cell by interacting with the heterotrimeric G-proteins, and they thereby participate in many aspects of regulation. Cellular responses to agonists of these receptors are usually rapidly attenuated. Mechanisms of signal attenuation include removal of agonists from the extracellular fluid, receptor desensitization, endocytosis and down-regulation. Agonists are removed by dilution, uptake by transporters and enzymic degradation. Receptor desensitization is mediated by receptor phosphorylation by G-protein receptor kinases and second-messenger kinases, interaction of phosphorylated receptors with arrestins and receptor uncoupling from G-proteins. Agonist-induced receptor endocytosis also contributes to desensitization by depleting the cell surface of high-affinity receptors, and recycling of internalized receptors contributes to resensitization of cellular responses. Receptor down-regulation is a form of desensitization that occurs during continuous, long-term exposure of cells to receptor agonists. Down-regulation, which may occur during the development of drug tolerance, is characterized by depletion of the cellular receptor content, and is probably mediated by alterations in the rates of receptor degradation and synthesis. These regulatory mechanisms are important, as they govern the ability of cells to respond to agonists. A greater understanding of the mechanisms that modulate signalling may lead to the development of new therapies and may help to explain the mechanism of drug tolerance.

Indexed as

AnimalsGTP-Binding ProteinsHumansReceptors, Cell SurfaceSignal TransductionGTP-Binding ProteinsReceptors, Cell Surface

Identifiers

PMID9078236
PMCPMC1218151
OpenAlexW1832014310

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.