ReviewNature reviews. Endocrinology2011
G protein-coupled receptors: mutations and endocrine diseases.
Review in Nature reviews. Endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 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
78 citing papers in PubMed, 164 citations in OpenAlex.
- Adhesion GPCR-induced ectocytosis mediates intercellular GPCR signal propagation.Nature chemical biology · 2026Article
- G protein-coupled receptor SmGPCR9 interacts with neuropeptides and controls spermatogenesis in Schistosoma mansoni.PLoS pathogens · 2026Article
- Mechanisms of primary failure of eruption: a new model of multidimensional framework.Progress in orthodontics · 2025Review
- A small molecule enhances arrestin-3 binding to the βCommunications chemistry · 2025Article
- In search of a photoswitchable drug for serotonin receptors: a molecular dynamics simulation study.RSC advances · 2025Article
- Regulation of Immune-Related Gene Expression by Salinity-Induced HPI Axis in Large Yellow Croaker,International journal of molecular sciences · 2025Article
- Insights into GLP-1 and insulin secretion mechanisms in pasireotide-induced hyperglycemia highlight effectiveness of Gs-targeting diabetes treatment.Scientific reports · 2025Article
- Cell-cell communication: new insights and clinical implications.Signal transduction and targeted therapy · 2024Review
- Know your molecule: pharmacological characterization of drug candidates to enhance efficacy and reduce late-stage attrition.Nature reviews. Drug discovery · 2024Review
- Understanding the genetic complexity of puberty timing across the allele frequency spectrum.Nature genetics · 2024Article
- Methylome analysis in girls with idiopathic central precocious puberty.Clinical epigenetics · 2024Article
- Editorial: Pharmacology of endocrine related GPCRs.Frontiers in endocrinology · 2024Article
- Ligand-Free Signaling of G-Protein-Coupled Receptors: Physiology, Pharmacology, and Genetics.Molecules (Basel, Switzerland) · 2023Review
- LGR4: A New Receptor Member in Endocrine and Metabolic Diseases.Endocrine reviews · 2023Review
- Alcohol-Related Liver Disease: An Overview on Pathophysiology, Diagnosis and Therapeutic Perspectives.Biomedicines · 2022Review
- Yeast-based directed-evolution for high-throughput structural stabilization of G protein-coupled receptors (GPCRs).Scientific reports · 2022Article
- Trafficking-defective mutant PROKR2 cycles between endoplasmic reticulum and Golgi to attenuate endoplasmic reticulum stress.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Mechanical regulation of bone remodeling.Bone research · 2022Review
- G protein-coupled receptors that influence lifespan of human and animal models.Biogerontology · 2022Review
- Whole-Exome Sequencing in Idiopathic Short Stature: Rare Mutations Affecting Growth.Journal of pediatric genetics · 2021Article
18 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Over the past 20 years, naturally occurring mutations that affect G protein-coupled receptors (GPCRs) have been identified, mainly in patients with endocrine diseases. The study of loss-of-function or gain-of-function mutations has contributed to our understanding of the pathophysiology of several diseases with classic hypophenotypes or hyperphenotypes of the target endocrine organs, respectively. Simultaneously, study of the mutant receptors ex vivo was instrumental in delineating the relationships between the structure and function of these important physiological and pharmacological molecules. Now that access to the crystallographic structure of a few GPCRs is available, the mechanics of these receptors can be studied at the atomic level. Progress in the fields of cell biology, molecular pharmacology and proteomics has also widened our view of GPCR functions. Initially considered simply as guanine nucleotide exchange factors capable of activating G protein-dependent regulatory cascades, GPCRs are now known to display several additional characteristics, each susceptible to alterations by disease-causing mutations. These characteristics include functionally important basal activity of the receptor; differential activation of various G proteins; differential activation of G protein-dependent and independent effects (biased agonism); interaction with proteins that modify receptor function; dimerization-dependent effects; and interaction with allosteric modulators. This Review attempts to illustrate how natural mutations of GPCR could contribute to our understanding of these novel facets of GPCR biology.
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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.