Evidence map›Paper›PMID 19133996›Full record

ArticleBritish journal of pharmacology2009

Do gene polymorphisms alone or in combination affect the function of human beta3-adrenoceptors?

Wim Vrydag, Astrid E Alewijnse, Martin C Michel

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

21 citing papers in PubMed, 41 citations in OpenAlex.

  1. Trial
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  6. Functional Characterization of the Obesity-Linked Variant of the βInternational journal of molecular sciences · 2021
    Article
  7. Article
  8. Agonist-induced desensitisation of βBritish journal of pharmacology · 2019
    Review
  9. Article
  10. Article
  11. How β3 -adrenoceptor-selective is mirabegron?British journal of pharmacology · 2016
    Article
  12. Article
  13. Article
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  15. Article
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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 2 institutions in 1 country.

Wim VrydagDepartment of Pharmacology and Pharmacotherapy, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
Astrid E Alewijnse
Martin C Michel
University of Amsterdam · NLAcademic Medical Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposebeta(3)-Adrenoceptors mediate many important physiological functions, for example, in the urinary bladder. The corresponding gene is polymorphic, and the W64R (Trp64Arg) single nucleotide polymorphism has been associated with disease states such as obesity, type 2 diabetes and bladder dysfunction. While these clinical data suggest that the 64R variant is hypofunctional, previous in vitro studies in which this variant was generated by site-directed mutagenesis and subsequent transfection have not consistently confirmed this. EXPERIMENTAL APPROACH: We transfected the wild-type human beta(3)-adrenoceptor and the 64R variant and also the more recently discovered 265M and 306F variants as well as 64R/265M and 64R/306F double mutants into human embryonic kidney cells and selected clones expressing the receptors at a density of about 100 fmol mg protein(-1). Receptor activation was measured by cAMP accumulation and ligand affinity by radioligand binding. Desensitisation was assessed as alterations of cAMP responses after prolonged agonist treatment. KEY

resultsNeither mutated receptor exhibited alterations in efficacy or potency for cAMP accumulation for any of five agonists (isoprenaline, noradrenaline, YM 178, FK 4664, CGP 12 177). In competition binding studies, the mutations did not affect the ability of any agonist to bind to the receptor. Wild-type receptors and the 64R variant exhibited similar isoprenaline-induced functional desensitization during a 24 h treatment. CONCLUSIONS AND IMPLICATIONS: None of the polymorphisms tested here significantly altered the interaction of isoprenaline, noradrenaline, YM 178, FK 4664 or CGP 12 177 with the human beta(3)-adrenoceptor when expressed at near physiological levels in a human cell line.

Indexed as

Polymorphism, Single NucleotideAcetanilidesAdrenergic beta-3 Receptor AgonistsAdrenergic beta-AgonistsBinding, CompetitiveBiphenyl CompoundsCell LineCyclic AMPHumansIsoproterenolMutagenesis, Site-DirectedNorepinephrinePhenethylaminesPropanolaminesRadioligand AssayReceptors, Adrenergic, beta-34'-(2-((2-(3-chlorophenyl)-2-hydroxyethyl)amino)ethyl)-3-methoxybiphenyl-4-carboxylic acidAcetanilidesAdrenergic beta-3 Receptor AgonistsAdrenergic beta-AgonistsBiphenyl CompoundsCGP 12177Cyclic AMPIsoproterenolmirabegronNorepinephrinePhenethylaminesPropanolaminesReceptors, Adrenergic, beta-3Thiazoles

Identifiers

PMID19133996
PMCPMC2697764
OpenAlexW2167373815

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.