ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
GPR56-regulated granule cell adhesion is essential for rostral cerebellar development.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 139 citations in OpenAlex.
- The therapeutic potential of orphan adhesion G-protein-coupled receptors.Nature reviews. Drug discovery · 2026Review
- Self-cleavage-dependent and -independent functions ofProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Transcriptomics and Phenotypic Analysis ofInternational journal of molecular sciences · 2023Article
- Multi-Omics Analysis of Glioblastoma and Glioblastoma Cell Line: Molecular Insights Into the Functional Role of GPR56 and TG2 in Mesenchymal Transition.Frontiers in oncology · 2022Article
- Role of ADGRG1/GPR56 in Tumor Progression.Cells · 2021Review
- The role of GPR56/ADGRG1 in health and disease.Biomedical journal · 2021Review
- Weighted gene co-expression network analysis identified underlying hub genes and mechanisms in the occurrence and development of viral myocarditis.Annals of translational medicine · 2020Article
- GAIN domain-mediated cleavage is required for activation of G protein-coupled receptor 56 (GPR56) by its natural ligands and a small-molecule agonist.The Journal of biological chemistry · 2019Article
- Adhesion G protein-coupled receptors: opportunities for drug discovery.Nature reviews. Drug discovery · 2019Article
- Mitotic granule cell precursors undergo highly dynamic morphological transitions throughout the external germinal layer of the chick cerebellum.Scientific reports · 2019Article
- Genetic basis of functional variability in adhesion G protein-coupled receptors.Scientific reports · 2019Article
- A de novo variant in ADGRL2 suggests a novel mechanism underlying the previously undescribed association of extreme microcephaly with severely reduced sulcation and rhombencephalosynapsis.Acta neuropathologica communications · 2018Article
- Moving into shape: cell migration during the development and histogenesis of the cerebellum.Histochemistry and cell biology · 2018Review
- Cancer Cell Mechanics: Adhesion G Protein-coupled Receptors in Action?Frontiers in oncology · 2018Article
- Disease-associated extracellular loop mutations in the adhesion G protein-coupled receptor G1 (ADGRG1; GPR56) differentially regulate downstream signaling.The Journal of biological chemistry · 2017Article
- Structural Basis for Regulation of GPR56/ADGRG1 by Its Alternatively Spliced Extracellular Domains.Neuron · 2016Article
- Adhesion GPCRs in Tumorigenesis.Handbook of experimental pharmacology · 2016Review
- Review
- High-level Gpr56 expression is dispensable for the maintenance and function of hematopoietic stem and progenitor cells in mice.Stem cell research · 2015Article
- ERBB3-mediated regulation of Bergmann glia proliferation in cerebellar lamination.Development (Cambridge, England) · 2015Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Mutations in GPR56, an orphan G-protein-coupled receptor (GPCR), cause bilateral frontoparietal polymicrogyria (BFPP), a disorder characterized by mental retardation, seizures, motor developmental delay, and ataxia. BFPP patients have structural abnormalities of the cerebral cortex, cerebellum, and pons. To shed light on the function of GPR56 and the anatomical and behavioral defects underlying BFPP, we analyzed the cerebellum of mice lacking this GPCR. Gpr56(-/-) mice display a severe malformation of the rostral cerebellum that develops perinatally. Defects involve fusion of adjacent lobules, disrupted layering of neurons and glia, and fragmentation of the pial basement membrane. At the age of defect onset, GPR56 expression is restricted specifically to developing granule cells in the rostral cerebellum, suggesting that GPR56 regulates properties of these cells. Indeed, granule cells from the rostral region of perinatal Gpr56(-/-) cerebella show loss of adhesion to extracellular matrix molecules of the pial basement membrane. Interference RNA-mediated knockdown of GPR56 recapitulates the loss of adhesion seen in knock-outs, and reexpression of GPR56 rescues the adhesion defect in knock-out granule cells. Loss of GPR56 does not affect cell proliferation, migration, or neurite outgrowth. These studies establish a novel role for GPR56 in the adhesion of developing neurons to basal lamina molecules and suggest that this adhesion is critical for maintenance of the pia and proper cerebellar morphogenesis.
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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.