ArticleThe Journal of biological chemistry2013
Structural and pharmacological characterization of novel potent and selective monoclonal antibody antagonists of glucose-dependent insulinotropic polypeptide receptor.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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.
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.
Who cites it
45 citing papers in PubMed, 83 citations in OpenAlex.
- GIP(3-30)NHDiabetologia · 2018Trial
- GIPR signaling modulates PYY-induced hypophagia and malaise in rodents.Molecular metabolism · 2026Article
- The evolution of the therapeutic concept 'GIP receptor antagonism'.Frontiers in endocrinology · 2025Review
- The role of GIPR in food intake control.Frontiers in endocrinology · 2025Review
- Discovery of Therapeutic Antibodies Targeting Complex Multi-Spanning Membrane Proteins.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2024Review
- Activation of Gs signaling in mouse enteroendocrine K cells greatly improves obesity- and diabetes-related metabolic deficits.The Journal of clinical investigation · 2024Article
- Does glucose-dependent insulinotropic polypeptide receptor blockade as well as agonism have a role to play in management of obesity and diabetes?The Journal of endocrinology · 2024Review
- Technologies for the discovery of G protein-coupled receptor-targeting biologics.Current opinion in biotechnology · 2024Review
- Pharmacological characterisation of erenumab, Aimovig, at two calcitonin gene-related peptide responsive receptors.British journal of pharmacology · 2024Article
- Relevance and consequence of chronic inflammation for obesity development.Molecular and cellular pediatrics · 2023Review
- An integrated platform approach enables discovery of potent, selective and ligand-competitive cyclic peptides targeting the GIP receptor.Chemical science · 2022Article
- Review
- Targeting the GIPR for obesity: To agonize or antagonize? Potential mechanisms.Molecular metabolism · 2021Review
- Detection of genome-edited and endogenously expressed G protein-coupled receptors.The FEBS journal · 2021Review
- Article
- Antioxidant Activity, Molecular Docking, Quantum Studies andFrontiers in pharmacology · 2021Article
- Gut Hormone GIP Induces Inflammation and Insulin Resistance in the Hypothalamus.Endocrinology · 2020Article
- Perspective: Implications of Ligand-Receptor Binding Kinetics for Therapeutic Targeting of G Protein-Coupled Receptors.ACS pharmacology & translational science · 2020Review
- Function-based high-throughput screening for antibody antagonists and agonists against G protein-coupled receptors.Communications biology · 2020Article
- Pharmacological antagonism of the incretin system protects against diet-induced obesity.Molecular metabolism · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucose-dependent insulinotropic polypeptide (GIP) is an endogenous hormonal factor (incretin) that, upon binding to its receptor (GIPr; a class B G-protein-coupled receptor), stimulates insulin secretion by beta cells in the pancreas. There has been a lack of potent inhibitors of the GIPr with prolonged in vivo exposure to support studies on GIP biology. Here we describe the generation of an antagonizing antibody to the GIPr, using phage and ribosome display libraries. Gipg013 is a specific competitive antagonist with equally high potencies to mouse, rat, dog, and human GIP receptors with a Ki of 7 nm for the human GIPr. Gipg013 antagonizes the GIP receptor and inhibits GIP-induced insulin secretion in vitro and in vivo. A crystal structure of Gipg013 Fab in complex with the human GIPr extracellular domain (ECD) shows that the antibody binds through a series of hydrogen bonds from the complementarity-determining regions of Gipg013 Fab to the N-terminal α-helix of GIPr ECD as well as to residues around its highly conserved glucagon receptor subfamily recognition fold. The antibody epitope overlaps with the GIP binding site on the GIPr ECD, ensuring competitive antagonism of the receptor. This well characterized antagonizing antibody to the GIPr will be useful as a tool to further understand the biological roles of GIP.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.