ArticleNature communications2015
The adhesion G protein-coupled receptor GPR56 is a cell-autonomous regulator of oligodendrocyte development.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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Who cites it
81 citing papers in PubMed, 141 citations in OpenAlex.
- The therapeutic potential of orphan adhesion G-protein-coupled receptors.Nature reviews. Drug discovery · 2026Review
- Adhesion G protein-coupled receptors.Pharmacological reviews · 2026Review
- The expanding roles of adhesion GPCRs in neural circuit assembly.Molecules and cells · 2026Review
- CSF proteomics identifies ADGRG1 as a predictive biomarker of intrathecal immune checkpoint inhibitor response in leptomeningeal metastasis.Journal for immunotherapy of cancer · 2026Article
- G-protein-coupled receptor ADGRG1 drives a protective microglial state in Alzheimer's disease through MYC activation.Neuron · 2025Article
- Spatiotemporal profiling of adhesion G protein-coupled receptors in developing mouse and human pancreas reveals a role for GPR56 in islet development.Cellular and molecular life sciences : CMLS · 2025Article
- Genetic deletion of G protein-coupled receptor 56 aggravates traumatic brain injury through the microglial CCL3/4/5 upregulation targeted to CCR5.Cell death & disease · 2025Article
- Loss of cardiomyocyte-specific adhesion G-protein-coupled receptor G1 (ADGRG1/GPR56) promotes pressure overload-induced heart failure.Bioscience reports · 2024Article
- Single-nucleus sequencing reveals enriched expression of genetic risk factors in extratelencephalic neurons sensitive to degeneration in ALS.Nature aging · 2024Article
- Regulators of Oligodendrocyte Differentiation.Cold Spring Harbor perspectives in biology · 2024Review
- The aminosteroid U73122 promotes oligodendrocytes generation and myelin formation.Acta pharmacologica Sinica · 2024Article
- The Schwann cell-specific G-protein Gαo (Gnao1) is a cell-intrinsic controller contributing to the regulation of myelination in peripheral nerve system.Acta neuropathologica communications · 2024Article
- GPR56, an Adhesion GPCR with Multiple Roles in Human Diseases, Current Status and Future Perspective.Current drug targets · 2024Review
- Primary cilia control oligodendrocyte precursor cell proliferation in white matter injury via Hedgehog-independent CREB signaling.Cell reports · 2023Article
- Hexahydroquinoline Derivatives Are Selective Agonists for the Adhesion G Protein-Coupled Receptor ADGRG1/GPR56.Molecular pharmacology · 2023Article
- Stalled oligodendrocyte differentiation in IDH-mutant gliomas.Genome medicine · 2023Article
- Ablation of GPR56 Causes β-Cell Dysfunction by ATP Loss through Mistargeting of Mitochondrial VDAC1 to the Plasma Membrane.Biomolecules · 2023Article
- Adhesion G protein-coupled receptors: structure, signaling, physiology, and pathophysiology.Physiological reviews · 2022Review
- A Glance at the Molecules That Regulate Oligodendrocyte Myelination.Current issues in molecular biology · 2022Review
- Microglial GPR56 is the molecular target of maternal immune activation-induced parvalbumin-positive interneuron deficits.Science advances · 2022Article
21 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
Mutations in GPR56, a member of the adhesion G protein-coupled receptor family, cause a human brain malformation called bilateral frontoparietal polymicrogyria (BFPP). Magnetic resonance imaging (MRI) of BFPP brains reveals myelination defects in addition to brain malformation. However, the cellular role of GPR56 in oligodendrocyte development remains unknown. Here, we demonstrate that loss of Gpr56 leads to hypomyelination of the central nervous system in mice. GPR56 levels are abundant throughout early stages of oligodendrocyte development, but are downregulated in myelinating oligodendrocytes. Gpr56-knockout mice manifest with decreased oligodendrocyte precursor cell (OPC) proliferation and diminished levels of active RhoA, leading to fewer mature oligodendrocytes and a reduced number of myelinated axons in the corpus callosum and optic nerves. Conditional ablation of Gpr56 in OPCs leads to a reduced number of mature oligodendrocytes as seen in constitutive knockout of Gpr56. Together, our data define GPR56 as a cell-autonomous regulator of oligodendrocyte development.
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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.