Evidence map›Paper›PMID 29249361›Full record

ArticleCell2018

Pharmacogenomics of GPCR Drug Targets.

Alexander S Hauser, Sreenivas Chavali, Ikuo Masuho, Leonie J Jahn, Kirill A Martemyanov, David E Gloriam, M Madan Babu

Open access · hybridAbstract read
In one paragraph

Article in Cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 336 papers.

0numbers the graph read from it
0cells of the map it votes in
336citing papers in PubMed
25.5field-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

336 citing papers in PubMed, 642 citations in OpenAlex.

  1. Article
  2. Article
  3. The GPCRDiabetologia · 2026
    Article
  4. Review
  5. Schizophrenia: from mechanism to therapy.Science China. Life sciences · 2026
    Review
  6. Article
  7. Molecular mechanism of allosteric modulation of opioid receptors.Signal transduction and targeted therapy · 2026
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. GPCR Heterodimers: Implications for Biased Signaling.Handbook of experimental pharmacology · 2026
    Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 3 countries.

Alexander S HauserMRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK; Department of Drug Design and Pharmacology, University of Copenhagen, Universitetsparken 2, 2100 Copenhagen, Denmark. Electronic address: alexander.hauser@sund.ku.dk.
Sreenivas ChavaliMRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK.
Ikuo MasuhoDepartment of Neuroscience, The Scripps Research Institute Florida, Jupiter, FL 33458, USA.
Leonie J JahnThe Novo Nordisk Foundation Center for Biosustainability, Technical University Denmark, Kemitorvet 2800 Kgs. Lyngby, Denmark.
Kirill A MartemyanovDepartment of Neuroscience, The Scripps Research Institute Florida, Jupiter, FL 33458, USA.
David E GloriamDepartment of Drug Design and Pharmacology, University of Copenhagen, Universitetsparken 2, 2100 Copenhagen, Denmark.
M Madan BabuMRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK. Electronic address: madanm@mrc-lmb.cam.ac.uk.
MRC Laboratory of Molecular Biology · GBScripps Research Institute · USNovo Nordisk Foundation · DKUniversity of Copenhagen · DK

Funding

Regulation of Striatal Signaling by RGS ProteinsR01DA036596 · NIDA · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI Kirill A. Martemyanov · 2014 to 2026
$6.5M
Molecular Basis of RGS Protein Function in the StriatumK02DA026405 · NIDA · UNIVERSITY OF MINNESOTA · PI MARTEMYANOV, KIRILL A. · 2009 to 2019
$1.2M
European Research Council 639125Medical Research Council MC_U105185859NIDA NIH HHS K02 DA026405NIDA NIH HHS R01 DA036596
6 · The paper itself

Abstract

Natural genetic variation in the human genome is a cause of individual differences in responses to medications and is an underappreciated burden on public health. Although 108 G-protein-coupled receptors (GPCRs) are the targets of 475 (∼34%) Food and Drug Administration (FDA)-approved drugs and account for a global sales volume of over 180 billion US dollars annually, the prevalence of genetic variation among GPCRs targeted by drugs is unknown. By analyzing data from 68,496 individuals, we find that GPCRs targeted by drugs show genetic variation within functional regions such as drug- and effector-binding sites in the human population. We experimentally show that certain variants of μ-opioid and Cholecystokinin-A receptors could lead to altered or adverse drug response. By analyzing UK National Health Service drug prescription and sales data, we suggest that characterizing GPCR variants could increase prescription precision, improving patients' quality of life, and relieve the economic and societal burden due to variable drug responsiveness. VIDEO ABSTRACT.

Indexed as

Pharmacogenomic VariantsSoftwareBinding SitesDrug PrescriptionsHEK293 CellsHumansPharmacogeneticsProtein BindingReceptors, G-Protein-CoupledReceptors, G-Protein-Coupledclinical trialdrug responseeconomic burdenFDA approved drugsGPCRnatural variationopioid receptorpersonalized medicinepharmacogenomicspolymorphism

Identifiers

PMID29249361
PMCPMC5766829
OpenAlexW2774455409

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.