ArticleThe Journal of biological chemistry2011
Disease-associated GPR56 mutations cause bilateral frontoparietal polymicrogyria via multiple mechanisms.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 81 citations in OpenAlex.
- Laminar pattern disruption in fetal incipient polymicrogyria: insights from post-mortem magnetic resonance imaging and neuropathological correlation.Pediatric radiology · 2026Article
- Adhesion G protein-coupled receptors.Pharmacological reviews · 2026Review
- GPR56/ADGRG1 induces biased Rho-ROCK-MLC and JAK-STAT3 signaling to promote amoeboid-like morphology and IL-6 upregulation in melanoma cells.Cell communication and signaling : CCS · 2025Article
- Article
- The G Protein-Coupled Receptor GPR56 Is an Inhibitory Checkpoint for NK Cell Migration.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Dysfunction of the adhesion G protein-coupled receptor latrophilin 1 (ADGRL1/LPHN1) increases the risk of obesity.Signal transduction and targeted therapy · 2024Article
- Mesenchymal Transglutaminase 2 Activates Epithelial ADAM17: Link to G-Protein-Coupled Receptor 56 (ADGRG1) Signalling.International journal of molecular sciences · 2024Article
- GPR56, an Adhesion GPCR with Multiple Roles in Human Diseases, Current Status and Future Perspective.Current drug targets · 2024Review
- Hexahydroquinoline Derivatives Are Selective Agonists for the Adhesion G Protein-Coupled Receptor ADGRG1/GPR56.Molecular pharmacology · 2023Article
- Review
- GPR97 triggers inflammatory processes in human neutrophils via a macromolecular complex upstream of PAR2 activation.Nature communications · 2022Article
- Adhesion G protein-coupled receptors: structure, signaling, physiology, and pathophysiology.Physiological reviews · 2022Review
- Adhesion G protein-coupled receptor gluing action guides tissue development and disease.Journal of molecular medicine (Berlin, Germany) · 2022Review
- Mechanistic Understanding of the Palmitoylation of GPharmaceutics · 2022Article
- CDK7/12/13 inhibition targets an oscillating leukemia stem cell network and synergizes with venetoclax in acute myeloid leukemia.EMBO molecular medicine · 2022Article
- Article
- Novel compound heterozygousWorld journal of clinical cases · 2022Article
- Play the plug: How bacteria modify recognition by host receptors?Frontiers in microbiology · 2022Article
- Article
- Crucial contribution of GPR56/ADGRG1, expressed by breast cancer cells, to bone metastasis formation.Cancer science · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Loss-of-function mutations in the gene encoding G protein-coupled receptor 56 (GPR56) lead to bilateral frontoparietal polymicrogyria (BFPP), an autosomal recessive disorder affecting brain development. The GPR56 receptor is a member of the adhesion-GPCR family characterized by the chimeric composition of a long ectodomain (ECD), a GPCR proteolysis site (GPS), and a seven-pass transmembrane (7TM) moiety. Interestingly, all identified BFPP-associated missense mutations are located within the extracellular region of GPR56 including the ECD, GPS, and the extracellular loops of 7TM. In the present study, a detailed molecular and functional analysis of the wild-type GPR56 and BFPP-associated point mutants shows that individual GPR56 mutants most likely cause BFPP via different combination of multiple mechanisms. These include reduced surface receptor expression, loss of GPS proteolysis, reduced receptor shedding, inability to interact with a novel protein ligand, and differential distribution of the 7TM moiety in lipid rafts. These results provide novel insights into the cellular functions of GPR56 receptor and reveal molecular mechanisms whereby GPR56 mutations induce BFPP.
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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.