ArticleThe Journal of biological chemistry2014
GPR37 protein trafficking to the plasma membrane regulated by prosaposin and GM1 gangliosides promotes cell viability.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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Who cites it
25 citing papers in PubMed, 43 citations in OpenAlex.
- Bi-allelic loss-of-function variants in JKAMP cause a neurodevelopmental syndrome associated with dysregulation of GPR37 trafficking.American journal of human genetics · 2026Article
- Review
- Intranasal administration of recombinant prosaposin attenuates neuronal apoptosis through GPR37/PI3K/Akt/ASK1 pathway in MCAO rats.Experimental neurology · 2024Article
- GPR37 and its neuroprotective mechanisms: bridging osteocalcin signaling and brain function.Frontiers in cell and developmental biology · 2024Review
- Orphan G Protein-Coupled Receptor GPR37 as an Emerging Therapeutic Target.ACS chemical neuroscience · 2023Review
- Article
- Mouse Mutants ofInternational journal of molecular sciences · 2022Review
- The Effect of Early Life Stress on Emotional Behaviors in GPR37KO Mice.International journal of molecular sciences · 2021Article
- GM1 Is Cytoprotective in GPR37-Expressing Cells and Downregulates Signaling.International journal of molecular sciences · 2021Article
- Identification of the GlialCAM interactome: the G protein-coupled receptors GPRC5B and GPR37L1 modulate megalencephalic leukoencephalopathy proteins.Human molecular genetics · 2021Article
- GPR37 modulates progenitor cell dynamics in a mouse model of ischemic stroke.Experimental neurology · 2021Article
- Transcriptomics-Based Phenotypic Screening Supports Drug Discovery in Human Glioblastoma Cells.Cancers · 2021Article
- Pro-cathepsin D, Prosaposin, and Progranulin: Lysosomal Networks in Parkinsonism.Trends in molecular medicine · 2020Review
- GPCRs, G Proteins, and Their Impact on β-cell Function.Comprehensive Physiology · 2020Review
- Quantitative Proteomics Reveal an Altered Pattern of Protein Expression in Brain Tissue from Mice Lacking GPR37 and GPR37L1.Journal of proteome research · 2020Article
- Deficits in Motor Performance, Neurotransmitters and Synaptic Plasticity in Elderly and Experimental Parkinsonian Mice Lacking GPR37.Frontiers in aging neuroscience · 2020Article
- Protective effects of GPR37FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- GPR37 and GPR37L1 differently interact with dopamine 2 receptors in live cells.Neuropharmacology · 2019Article
- The Role of Lipids in Parkinson's Disease.Cells · 2019Review
- Spatiotemporal Control of GPR37 Signaling and Its Behavioral Effects by Optogenetics.Frontiers in molecular neuroscience · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The subcellular distribution of the G protein-coupled receptor GPR37 affects cell viability and is implicated in the pathogenesis of parkinsonism. Intracellular accumulation and aggregation of GPR37 cause cell death, whereas GPR37 located in the plasma membrane provides cell protection. We define here a pathway through which the recently identified natural ligand, prosaposin, promotes plasma membrane association of GPR37. Immunoabsorption of extracellular prosaposin reduced GPR37(tGFP) surface density and decreased cell viability in catecholaminergic N2a cells. We found that GPR37(tGFP) partitioned in GM1 ganglioside-containing lipid rafts in the plasma membrane of live cells. This partitioning required extracellular prosaposin and was disrupted by lipid raft perturbation using methyl-β-cyclodextrin or cholesterol oxidase. Moreover, complex formation between GPR37(tGFP) and the GM1 marker cholera toxin was observed in the plasma membrane. These data show functional association between GPR37, prosaposin, and GM1 in the plasma membrane. These results thus tie together the three previously defined components of the cellular response to insult. Our findings identify a mechanism through which the receptor's natural ligand and GM1 may protect against toxic intracellular GPR37 aggregates observed in parkinsonism.
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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.