Evidence map›Paper›PMID 23864649›Full record

ReviewMolecular endocrinology (Baltimore, Md.)2013

Minireview: Signal bias, allosterism, and polymorphic variation at the GLP-1R: implications for drug discovery.

Cassandra Koole, Emilia E Savage, Arthur Christopoulos, Laurence J Miller, Patrick M Sexton, Denise Wootten

Open access · greenAbstract readReview
In one paragraph

Review in Molecular endocrinology (Baltimore, Md.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

23 citing papers in PubMed, 42 citations in OpenAlex.

  1. Trial
  2. The GPCRDiabetologia · 2026
    Article
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  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Optical Control of Insulin Secretion Using an Incretin Switch.Angewandte Chemie (International ed. in English) · 2015
    Article
  18. Article
  19. Review
  20. 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

6 authors at 2 institutions in 2 countries.

Cassandra KooleDepartment of Drug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville 3052, Victoria, Australia.
Emilia E Savage
Arthur Christopoulos
Laurence J Miller
Patrick M Sexton
Denise Wootten
Monash University · AUMayo Clinic in Arizona · US

Funding

SECRETIN RECEPTOR STRUCTURE, FUNCTION, AND REGULATIONR01DK046577 · NIDDK · MAYO CLINIC COLL OF MED, MAYO CLINIC AZ · PI MILLER, LAURENCE J · 1995 to 2013
$4.9M
Secretin Receptor Structure, Function and RegulationR56DK046577 · NIDDK · MAYO CLINIC ARIZONA · PI MILLER, LAURENCE J · 2014 to 2014
$154k
NIDDK NIH HHS DK046577NIDDK NIH HHS R01 DK046577NIDDK NIH HHS R56 DK046577
6 · The paper itself

Abstract

The glucagon-like peptide-1 receptor (GLP-1R) controls the physiological responses to the incretin hormone glucagon-like peptide-1 and is a major therapeutic target for the treatment of type 2 diabetes, owing to the broad range of effects that are mediated upon its activation. These include the promotion of glucose-dependent insulin secretion, increased insulin biosynthesis, preservation of β-cell mass, improved peripheral insulin action, and promotion of weight loss. Regulation of GLP-1R function is complex, with multiple endogenous and exogenous peptides that interact with the receptor that result in the activation of numerous downstream signaling cascades. The current understanding of GLP-1R signaling and regulation is limited, with the desired spectrum of signaling required for the ideal therapeutic outcome still to be determined. In addition, there are several single-nucleotide polymorphisms (used in this review as defining a natural change of single nucleotide in the receptor sequence; clinically, this is viewed as a single-nucleotide polymorphism only if the frequency of the mutation occurs in 1% or more of the population) distributed within the coding sequence of the receptor protein that have the potential to produce differential responses for distinct ligands. In this review, we discuss the current understanding of GLP-1R function, in particular highlighting recent advances in the field on ligand-directed signal bias, allosteric modulation, and probe dependence and the implications of these behaviors for drug discovery and development.

Indexed as

Allosteric RegulationAmino Acid SequenceDiabetes Mellitus, Type 2Drug DiscoveryGlucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorGlucoseHumansIncretinsInsulinInsulin SecretionMolecular Sequence DataPolymorphism, Single NucleotideReceptors, GlucagonSignal TransductionGLP1R protein, humanGlucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorGlucoseIncretinsInsulinReceptors, Glucagon

Identifiers

PMID23864649
PMCPMC3725346
OpenAlexW2018274594

What Socratic 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 Socratic graph.