Affinage

GPR37

Prosaposin receptor GPR37 · UniProt O15354

Length
613 aa
Mass
67.1 kDa
Annotated
2026-06-10
44 papers in source corpus 16 papers cited in narrative 20 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 9/9 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

GPR37 (Pael-R) is a seven-transmembrane G protein-coupled receptor expressed predominantly in the nervous system whose dysfunction links protein quality control to dopaminergic neurodegeneration (PMID:9144577, PMID:12150907). Although originally cloned for its similarity to the endothelin type B receptor, endothelins do not bind or activate it (PMID:9144577). GPR37 is intrinsically prone to misfolding: when unfolded or overexpressed it accumulates in the ER and triggers ER stress and selective dopaminergic neuron death, a phenotype demonstrated in Drosophila, in mouse and rat substantia nigra, and exacerbated by loss of the ER chaperone ORP150 (PMID:12670421, PMID:17116640, PMID:19348945). The receptor is a substrate of the Parkinson's disease E3 ubiquitin ligase Parkin, which ubiquitinates and degrades misfolded GPR37 to suppress ER stress-induced cell death; CHIP and Hsp70 act as co-factors that potentiate this ubiquitination, and the chaperone-associated proteins PACRG/Glup and thioredoxin further buffer GPR37 toxicity (PMID:12150907, PMID:14532270, PMID:17301052). A parallel ER-associated ligase, HRD1, independently ubiquitinates and degrades GPR37 and protects against its apoptotic accumulation (PMID:17059562). Loss of Parkin combined with GPR37 transgene expression causes early progressive loss of dopaminergic and noradrenergic neurons with UPR activation, establishing GPR37 accumulation downstream of Parkin loss as a cause of neurodegeneration (PMID:18691389). GPR37 surface trafficking is gated by its cysteine-rich C-terminal domain and its N-terminus, and is enhanced by N-terminal truncation, co-expression with dopamine D2 or adenosine A2A receptors, and binding of the PDZ scaffold syntenin-1, while PICK1 and GABARAPL2 bind its C-terminus and lower receptor levels (PMID:19799451, PMID:23398388, PMID:24749734). Once at the membrane, GPR37 functions as a Gi/o-coupled receptor activated by prosaptide/prosaposin, signaling through pertussis-toxin-sensitive ERK phosphorylation and inhibition of cAMP to confer cytoprotection against oxidative stress (PMID:23690594). GPR37 additionally regulates striatal dopamine metabolism (PMID:17889953), guides olfactory ensheathing cell and GnRH neuron migration in development (PMID:31143101), and serves as a receptor for lipid and peptide ligands in pain and immune contexts.

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 1997 Medium

    Cloning of an endothelin-receptor-like orphan GPCR resolved whether endothelins were its ligands, establishing GPR37 as a true orphan receptor.

    Evidence Radioligand binding, Ca2+ and cAMP assays in transfected COS7/HEK293 cells

    PMID:9144577

    Open questions at the time
    • No endogenous ligand identified at this stage
    • No cellular function or localization defined
  2. 2002 High

    Identification of GPR37 as a Parkin substrate connected an orphan GPCR to Parkinson's disease protein quality control, defining how misfolded GPR37 is cleared to prevent ER stress death.

    Evidence Yeast two-hybrid, Co-IP, in vitro ubiquitination and cell death assays; CHIP/Hsp70 complex reconstitution

    PMID:12150907

    Open questions at the time
    • Degradation studied in overexpression contexts
    • Physiological substrate role of folded receptor not addressed
  3. 2003 High

    In vivo genetic epistasis in Drosophila established that GPR37 accumulation selectively kills dopaminergic neurons and that Parkin acts upstream to suppress this toxicity.

    Evidence Drosophila transgenic gain- and loss-of-function with DA neuron counting

    PMID:12670421

    Open questions at the time
    • Mechanism of dopaminergic selectivity unresolved
    • Endogenous ligand and signaling not involved in toxicity readout
  4. 2003 Medium

    Discovery of PACRG/Glup as a chaperone-complex partner showed GPR37 handling involves Hsp70/Hsp90 machinery directing it to inclusion bodies or death.

    Evidence Co-IP, siRNA knockdown, cell viability and immunofluorescence

    PMID:14532270

    Open questions at the time
    • Single lab
    • In vivo relevance of inclusion formation not tested
  5. 2006 High

    Identification of HRD1 revealed a Parkin-independent ER-associated degradation route for GPR37, explaining parallel clearance of the misfolded receptor.

    Evidence Co-IP, in vitro ubiquitination, siRNA knockdown with caspase-3 readout

    PMID:17059562

    Open questions at the time
    • Relative contribution of HRD1 versus Parkin in vivo unquantified
  6. 2006 High

    In vivo overexpression in mouse substantia nigra established that GPR37 causes ER stress and dopamine-dependent neuron death, mechanistically separating ER stress and dopamine toxicity components.

    Evidence Adenoviral expression, Parkin and ORP150 KO mice, dopamine synthesis inhibition, IHC

    PMID:17116640

    Open questions at the time
    • Link between ER stress and dopamine toxicity not molecularly defined
  7. 2007 Medium

    Knockout and transgenic mice showed GPR37 regulates nigrostriatal dopamine levels and neurotoxin vulnerability, indicating a physiological role beyond misfolding toxicity.

    Evidence KO/Tg mice, HPLC dopamine/DOPAC, neurotoxin challenge

    PMID:17889953

    Open questions at the time
    • Mechanism linking GPR37 to dopamine handling unknown
    • Single lab
  8. 2007 Medium

    Thioredoxin was shown to suppress GPR37 toxicity through chaperone rather than antioxidant activity, refining the protein-folding basis of GPR37 neurotoxicity.

    Evidence Drosophila coexpression with TRX active-site mutagenesis, DA neuron and locomotor readouts

    PMID:17301052

    Open questions at the time
    • Direct TRX-GPR37 interaction not shown
    • Single lab
  9. 2008 High

    A Parkin KO × GPR37 transgenic double mutant placed GPR37 accumulation downstream of Parkin loss as causal for progressive neurodegeneration with UPR and complex I deficits.

    Evidence Double-mutant mice, stereology, UPR markers, dopamine HPLC, complex I assay

    PMID:18691389

    Open questions at the time
    • Whether complex I deficit is direct or secondary not resolved
  10. 2009 Medium

    Mapping of trafficking determinants showed N-terminal truncation, D2R/A2AR coexpression, and syntenin-1 binding promote GPR37 surface delivery, explaining how the misfolding-prone receptor reaches the membrane.

    Evidence Truncation constructs, flow cytometry, Co-IP, radioligand binding

    PMID:19799451

    Open questions at the time
    • Functional consequence of D2R heterocomplex on signaling unclear
    • Single lab
  11. 2009 Medium

    AAV overexpression in adult rat nigrostriatum reproduced selective dopaminergic loss and motor deficits, validating GPR37 accumulation as a mammalian PD-relevant lesion.

    Evidence rAAV2/6 delivery, IHC, behavioral tests, dopamine HPLC

    PMID:19348945

    Open questions at the time
    • Endogenous receptor levels in pathology not addressed
    • Single lab
  12. 2013 High

    Identification of prosaptide/prosaposin as agonists deorphanized GPR37, defining it as a Gi/o-coupled cytoprotective receptor signaling via ERK and cAMP inhibition.

    Evidence Endocytosis, radioligand binding, ERK with PTX, GTPγS, cAMP, siRNA, cell viability

    PMID:23690594

    Open questions at the time
    • Structural basis of ligand binding not defined
    • In vivo signaling outputs not mapped
  13. 2013 Medium

    The C-terminal cysteine-rich domain was shown to govern surface expression, signaling, and cytotoxicity, identifying a structural switch between toxic and functional receptor states.

    Evidence Cysteine deletion mutants, flow cytometry, apoptosis/death assays

    PMID:23398388

    Open questions at the time
    • Single lab
    • Native regulation of these cysteines unknown
  14. 2014 Medium

    PICK1 was identified as a PDZ partner that lowers GPR37 levels and reduces its toxicity proteasome-dependently, adding a scaffold-linked regulatory layer.

    Evidence GST pull-down from brain and cells, Co-IP, viability under rotenone, proteasome inhibition

    PMID:24749734

    Open questions at the time
    • Mechanism of PICK1-directed degradation unclear
    • Single lab
  15. 2018 Low

    GABARAPL2 binding to the GPR37 C-terminus implicated autophagy in regulating receptor levels.

    Evidence GST affinity chromatography, in-silico modeling, transfection/Western

    PMID:29496607

    Open questions at the time
    • Single pull-down method without rescue
    • Autophagic degradation not directly demonstrated
  16. 2019 Medium

    GPR37 signaling was found to drive olfactory ensheathing cell and GnRH neuron migration, establishing a developmental morphogenetic role.

    Evidence GPR37 KO mice, nasal explant inhibition, immunocytochemistry, PCR

    PMID:31143101

    Open questions at the time
    • Downstream migratory signaling pathway unknown
    • Single lab
  17. 2024 Medium

    Osteocalcin was shown to activate GPR37 in VTA GABAergic neurons to suppress THIK-1 channels via cAMP reduction, linking a bone-derived ligand to neuronal excitability and behavior.

    Evidence GPR37 KO and conditional KO, scRNA-seq, patch-clamp, chemogenetics, visual escape behavior (preprint)

    Open questions at the time
    • Preprint not yet peer-reviewed
    • Direct OCN-GPR37 binding not shown
  18. 2025 Medium

    GPR37 activation by lipid mediators in TRPV1-lineage sensory neurons and macrophages was shown to resolve nociceptive sensitization and promote efferocytosis, expanding its ligand repertoire to specialized pro-resolving mediators.

    Evidence Global and conditional GPR37 KO, intrathecal pharmacology, behavioral and Ca2+ imaging, macrophage efferocytosis (preprints)

    Open questions at the time
    • Preprints not yet peer-reviewed
    • Receptor coupling in these cell types not fully defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How GPR37 reconciles its misfolding-driven neurotoxic accumulation with its physiological ligand-activated cytoprotective and excitability-modulating signaling remains unresolved.
  • No structure of GPR37 with any ligand
  • Quantitative balance of degradation pathways in disease unknown
  • Mechanism linking same receptor to both death and protection unclear

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060089 molecular transducer activity 2 GO:0048018 receptor ligand activity 1
Localization
GO:0005783 endoplasmic reticulum 2 GO:0005886 plasma membrane 2
Pathway
R-HSA-392499 Metabolism of proteins 2 R-HSA-5357801 Programmed Cell Death 2 R-HSA-162582 Signal Transduction 1
Partners
DRD2GABARAPL2HRD1HSPA1APARK2PICK1STUB1SYNJ2BP
Complex memberships
Parkin–CHIP–Hsp70–GPR37 complex

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1997 GPR37 (hET(B)R-LP) encodes a 614-amino-acid seven-transmembrane GPCR with 52% similarity to endothelin type B receptor; when expressed in COS7 and HEK293 cells, recombinant hET(B)R-LP did not show significant binding of radiolabeled ET-1 or ET-3, and ET-1, ET-3, bombesin, and neuropeptide Y failed to produce Ca2+ mobilization or cAMP changes, indicating endothelins are NOT ligands for this receptor. Radioligand binding assay, Ca2+ mobilization assay, cAMP assay in transfected COS7/HEK293 cells Biochemical and biophysical research communications Medium 9144577
2002 GPR37 (Pael-R) is a substrate of the E3 ubiquitin ligase Parkin; Parkin specifically ubiquitinates unfolded/insoluble Pael-R and promotes its degradation, suppressing ER stress-induced cell death. Pael-R was identified as a Parkin-binding protein by yeast two-hybrid screening. Yeast two-hybrid, co-immunoprecipitation, in vitro ubiquitination assay, cell death assay Molecular cell High 12150907
2002 CHIP, Hsp70, Parkin, and GPR37 (Pael-R) form a complex in vitro and in vivo. CHIP promotes dissociation of Hsp70 from Parkin and Pael-R, facilitating Parkin-mediated Pael-R ubiquitination. CHIP enhanced Parkin-mediated in vitro ubiquitination of Pael-R even in the absence of Hsp70, acting as an E4-like co-factor. Co-immunoprecipitation, in vitro ubiquitination assay, in vitro complex reconstitution Molecular cell High 12150907
2003 Panneuronal expression of GPR37 (Pael-R) in Drosophila causes age-dependent selective degeneration of dopaminergic neurons; coexpression of Parkin degrades Pael-R and suppresses its toxicity. Interfering with endogenous Drosophila Parkin promotes Pael-R accumulation and augments its toxicity, establishing Parkin as epistatic to Pael-R in this pathway. Drosophila transgenic overexpression and loss-of-function, DA neuron counting, immunostaining Neuron High 12670421
2003 Glup/PACRG (product of gene adjacent to Parkin) forms a large molecular chaperone complex containing Hsp70 and Hsp90, interacts with Pael-R, suppresses Pael-R-induced cell death, and facilitates inclusion body formation when the proteasome is inhibited; Glup knockdown attenuated inclusion formation and promoted cell death. Co-immunoprecipitation, siRNA knockdown, cell viability assay, immunofluorescence The Journal of biological chemistry Medium 14532270
2006 HRD1, a ubiquitin ligase expressed in substantia nigra dopaminergic neurons, interacts with GPR37 (Pael-R) through the HRD1 proline-rich region, promotes ubiquitination and degradation of Pael-R, and protects against Pael-R-induced apoptosis. siRNA knockdown of endogenous HRD1 induced Pael-R accumulation and caspase-3 activation. Co-immunoprecipitation, in vitro ubiquitination assay, siRNA knockdown, caspase-3 activation assay Journal of neurochemistry High 17059562
2006 GPR37 (Pael-R) overexpression in mouse substantia nigra via adenoviral vectors caused ER stress and death of dopaminergic neurons in vivo. Dopaminergic neuronal death was enhanced in mice deficient in Parkin and the ER chaperone ORP150, and a dopamine synthesis inhibitor blocked neuronal death in parkin null mice, implicating both ER stress and dopamine toxicity in Pael-R-mediated neurodegeneration. Adenoviral in vivo expression, Parkin knockout mouse, ORP150 knockout mouse, pharmacological inhibition, immunohistochemistry Human molecular genetics High 17116640
2007 GPR37 (Pael-R) regulates dopamine metabolism in the nigrostriatal system: Pael-R knockout mice show ~60% striatal dopamine levels compared to wild-type, while Pael-R transgenic mice show increased striatal DOPAC and vesicular dopamine content. Pael-R transgenic nigrostriatal neurons are more vulnerable to PD-related neurotoxins. Knockout and transgenic mouse models, HPLC dopamine/DOPAC measurement, neurotoxin challenge Neuroscience research Medium 17889953
2007 Thioredoxin (TRX) suppresses Pael-R (GPR37)-induced neurotoxicity in Drosophila dopaminergic neurons; redox-defective TRX mutants still suppressed Pael-R toxicity, suggesting TRX chaperone activity (rather than antioxidant activity) is the primary mechanism of suppression. Drosophila transgenic coexpression, dopaminergic neuron counting, locomotor activity assay, mutagenesis of TRX active site The Journal of biological chemistry Medium 17301052
2008 Parkin knockout/Pael-R transgenic double-mutant mice display early and progressive loss of dopaminergic and noradrenergic neurons, activation of the unfolded protein response (UPR), upregulation of dopamine and metabolites, and reduced mitochondrial complex I activity later in life — establishing Pael-R accumulation downstream of Parkin loss as mechanistically causing neurodegeneration. Double-mutant mouse model (Parkin KO × Pael-R Tg), stereological neuron counting, UPR markers, dopamine HPLC, mitochondrial complex I activity assay Journal of neurochemistry High 18691389
2009 N-terminal truncation of GPR37 (removal of first 210 or all N-terminal amino acids) dramatically enhances plasma membrane surface expression. Coexpression with adenosine A2A receptor or dopamine D2 receptor increases GPR37 surface expression; full-length GPR37 associates with D2R by co-immunoprecipitation, modestly altering D2R agonist/antagonist affinity. GPR37 also specifically interacts with PDZ scaffold syntenin-1, dramatically increasing GPR37 surface expression in HEK-293 cells. N-terminal truncation constructs, flow cytometry surface expression assay, co-immunoprecipitation, radioligand binding assay Biochemistry Medium 19799451
2009 AAV-mediated overexpression of rat Pael-R (GPR37) in the nigrostriatal system of adult rats causes rapid insoluble accumulation of the receptor, severe loss of nigral dopaminergic neurons and nigrostriatal fibers, striatal dopamine depletion, and spontaneous motor impairments; GABAergic neurons of the globus pallidus were unaffected, demonstrating selective dopaminergic vulnerability. Recombinant AAV (rAAV2/6) in vivo gene delivery, immunohistochemistry, behavioral testing (cylinder and stepping tests), dopamine HPLC Neurobiology of disease Medium 19348945
2013 GPR37 and GPR37L1 are receptors for prosaptide (active fragment of prosaposin/sulfated glycoprotein-1). Prosaptide promotes endocytosis of GPR37 and GPR37L1, binds both receptors, induces ERK phosphorylation in a pertussis toxin-sensitive manner, stimulates 35S-GTPγS binding, and inhibits forskolin-stimulated cAMP production in a GPR37/GPR37L1-dependent manner. Full-length prosaposin also activates GPR37 signaling. siRNA knockdown of GPR37 or GPR37L1 attenuates prosaptide/prosaposin-mediated astrocyte protection against oxidative stress. Receptor endocytosis assay, radioligand binding, ERK phosphorylation assay with pertussis toxin, 35S-GTPγS binding, cAMP assay, siRNA knockdown, cell viability assay Proceedings of the National Academy of Sciences of the United States of America High 23690594
2013 The C-terminal cysteine-rich domain of GPR37 controls its plasma membrane expression, signaling, and cytotoxicity. Deletion of six cysteine residues in this region promoted GPR37 plasma membrane expression and signaling without affecting receptor internalization, and protected against GPR37-mediated apoptosis and cell death. Site-directed mutagenesis/deletion constructs, flow cytometry surface expression, cell death/apoptosis assays Journal of neurochemistry Medium 23398388
2014 PICK1 interacts with GPR37 (PAELR) via its PDZ domain binding to the C-terminal PDZ motif of PAELR. Pull-down assays confirmed PICK1 is retained by GST-fused C-terminal PAELR from both heterologous cells and rat brain tissue. PICK1 overexpression reduces PAELR expression levels and reduces PAELR-induced cell death during rotenone treatment in a proteasome-dependent manner. GST pull-down, co-immunoprecipitation from rat brain tissue and transfected cells, cell viability assay, proteasome inhibitor treatment Journal of neurochemistry Medium 24749734
2018 GABARAPL2 interacts with GPR37 (PAELR) via the GABAA binding site of GABARAPL2 and the cysteine-rich region (-CCCCCC-EEC) of the C-terminal of PAELR. Affinity chromatography confirmed Myc-GABARAPL2 is retained by GST-fused C-terminal PAELR. Transient transfection of GABARAPL2 reduces PAELR expression, suggesting autophagy-mediated regulation. GST affinity chromatography, in-silico modelling, transfection/Western blot Neuroscience letters Low 29496607
2019 GPR37 signaling is required for the migration of olfactory ensheathing cells and GnRH neurons in the developing mouse olfactory system. Inhibition of GPR37 signaling in nasal explants attenuated GnRH neuronal migration and OEC movement. GPR37-deficient mice showed decreased olfactory bulb nerve layer and attenuated/delayed GnRH neuron migration into the brain. GPR37 knockout mouse, nasal explant cultures with GPR37 inhibition, immunocytochemistry, PCR Frontiers in cellular neuroscience Medium 31143101
2024 Osteocalcin (OCN), a bone-derived protein, activates GPR37 in a subpopulation of VTA GABAergic neurons to decrease potassium currents via GPR37-induced cAMP reduction and subsequent suppression of THIK-1 (K2P13.1) channels, increasing neuronal excitability. Knockout of GPR37 or conditional knockout in VTA GABAergic neurons delayed rapid visual escape response; reconstituting OCN-GPR37 signaling in VTA restored normal response. GPR37 knockout and conditional knockout mice, single-cell transcriptomics, patch-clamp electrophysiology, chemogenetics (HM4Di), behavioral assay (visual escape) bioRxivpreprint Medium
2025 GPR37 activation in TRPV1-lineage sensory neurons at the spinal level erases nociceptive sensitization. Intrathecal GPR37 agonists (TX14A and protectin D1) dose-dependently inhibited capsaicin-induced nociception acutely and long-term, and produced 'unpriming' in the hyperalgesic priming model. Global GPR37 KO and conditional KO in TRPV1-lineage neurons abolished these effects. Ex vivo Ca2+ imaging showed i.th. TX14A rescued dorsal horn interneurons from long-term potentiation/depression. GPR37 global knockout, conditional knockout (TRPV1-Cre), intrathecal pharmacology, behavioral nociceptive assays, ex vivo Ca2+ imaging of dorsal horn neurons bioRxivpreprint Medium
2025 Protectin DX (PDX) activates GPR37 on macrophages to promote efferocytosis of apoptotic cells via calcium signaling. In a tibial fracture pain model, analgesic effects of PDX were abolished in Gpr37−/− mice. PDX binds GPR37 and induces calcium responses in peritoneal macrophages in a GPR37-dependent manner. GPR37 knockout mouse, in vivo fracture pain model, in vitro macrophage efferocytosis assay, calcium imaging, lipidomics bioRxivpreprint Medium

Source papers

Stage 0 corpus · 44 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2002 CHIP is associated with Parkin, a gene responsible for familial Parkinson's disease, and enhances its ubiquitin ligase activity. Molecular cell 405 12150907
2003 Parkin suppresses dopaminergic neuron-selective neurotoxicity induced by Pael-R in Drosophila. Neuron 301 12670421
2003 Parkin facilitates the elimination of expanded polyglutamine proteins and leads to preservation of proteasome function. The Journal of biological chemistry 231 12676955
2013 GPR37 and GPR37L1 are receptors for the neuroprotective and glioprotective factors prosaptide and prosaposin. Proceedings of the National Academy of Sciences of the United States of America 194 23690594
2006 Suppressive effects of 4-phenylbutyrate on the aggregation of Pael receptors and endoplasmic reticulum stress. Journal of neurochemistry 152 16539653
2004 Pael-R is accumulated in Lewy bodies of Parkinson's disease. Annals of neurology 125 14991825
2013 Pathway Analysis of ChIP-Seq-Based NRF1 Target Genes Suggests a Logical Hypothesis of their Involvement in the Pathogenesis of Neurodegenerative Diseases. Gene regulation and systems biology 117 24250222
2009 Identification of a novel Zn2+-binding domain in the autosomal recessive juvenile Parkinson-related E3 ligase parkin. The Journal of biological chemistry 109 19339245
2013 Endoplasmic reticulum stress and Parkinson's disease: the role of HRD1 in averting apoptosis in neurodegenerative disease. Oxidative medicine and cellular longevity 103 23710284
2003 Parkin: a multipurpose neuroprotective agent? Neuron 93 12691660
2006 Pael receptor induces death of dopaminergic neurons in the substantia nigra via endoplasmic reticulum stress and dopamine toxicity, which is enhanced under condition of parkin inactivation. Human molecular genetics 89 17116640
2006 A ubiquitin ligase HRD1 promotes the degradation of Pael receptor, a substrate of Parkin. Journal of neurochemistry 78 17059562
2012 Protective effects of 4-phenylbutyrate derivatives on the neuronal cell death and endoplasmic reticulum stress. Biological & pharmaceutical bulletin 69 22223342
2009 GPR37 surface expression enhancement via N-terminal truncation or protein-protein interactions. Biochemistry 60 19799451
2003 A product of the human gene adjacent to parkin is a component of Lewy bodies and suppresses Pael receptor-induced cell death. The Journal of biological chemistry 59 14532270
1997 A novel endothelin receptor type-B-like gene enriched in the brain. Biochemical and biophysical research communications 57 9144577
2003 Pael receptor, endoplasmic reticulum stress, and Parkinson's disease. Journal of neurology 55 14579121
2012 Mutation in Parkinson disease-associated, G-protein-coupled receptor 37 (GPR37/PaelR) is related to autism spectrum disorder. PloS one 48 23251443
2009 Targeted overexpression of the parkin substrate Pael-R in the nigrostriatal system of adult rats to model Parkinson's disease. Neurobiology of disease 48 19348945
2008 Pael-R transgenic mice crossed with parkin deficient mice displayed progressive and selective catecholaminergic neuronal loss. Journal of neurochemistry 48 18691389
2020 TGF-β/Smad3 Signalling Modulates GABA Neurotransmission: Implications in Parkinson's Disease. International journal of molecular sciences 44 31963327
2015 Drug Discovery Opportunities at the Endothelin B Receptor-Related Orphan G Protein-Coupled Receptors, GPR37 and GPR37L1. Frontiers in pharmacology 42 26635605
2007 Pael receptor is involved in dopamine metabolism in the nigrostriatal system. Neuroscience research 39 17889953
2008 Novel functions of ubiquitin ligase HRD1 with transmembrane and proline-rich domains. Journal of pharmacological sciences 35 18344614
2007 Thioredoxin suppresses Parkin-associated endothelin receptor-like receptor-induced neurotoxicity and extends longevity in Drosophila. The Journal of biological chemistry 35 17301052
2008 Immunohistochemical localization of a ubiquitin ligase HRD1 in murine brain. Journal of neuroscience research 34 18241051
2013 The Parkinson's disease-associated GPR37 receptor-mediated cytotoxicity is controlled by its intracellular cysteine-rich domain. Journal of neurochemistry 31 23398388
2017 Folding Underlies Bidirectional Role of GPR37/Pael-R in Parkinson Disease. Trends in pharmacological sciences 28 28629580
2014 A low level of GPR37 is associated with human hepatocellular carcinoma progression and poor patient survival. Pathology, research and practice 28 25169131
2016 Neuroprotection by Endoplasmic Reticulum Stress-Induced HRD1 and Chaperones: Possible Therapeutic Targets for Alzheimer's and Parkinson's Disease. Medical sciences (Basel, Switzerland) 19 29083378
2015 Adenosine A2A receptor-mediated control of pilocarpine-induced tremulous jaw movements is Parkinson's disease-associated GPR37 receptor-dependent. Behavioural brain research 17 25862943
2019 GPR37 Signaling Modulates Migration of Olfactory Ensheathing Cells and Gonadotropin Releasing Hormone Cells in Mice. Frontiers in cellular neuroscience 12 31143101
2012 [Molecular pharmacological studies on the protection mechanism against endoplasmic reticulum stress-induced neurodegenerative disease]. Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan 12 23208051
2014 The protein interacting with C-kinase (PICK1) interacts with and attenuates parkin-associated endothelial-like (PAEL) receptor-mediated cell death. Journal of neurochemistry 11 24749734
2016 [Physiological Roles of Ubiquitin Ligases Related to the Endoplasmic Reticulum]. Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan 8 27252059
2018 A novel modelling mechanism of PAEL receptor and GABARAPL2 interaction involved in Parkinson's disease. Neuroscience letters 7 29496607
2014 [Pharmacological studies on neurodegenerative diseases focusing on refolding and degradation of unfolded proteins in the endoplasmic reticulum]. Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan 7 24694815
2012 Downregulation of Pael-R expression in a Parkinson's disease cell model reduces apoptosis. Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia 6 22898202
2024 5-Phenyl valeric acid attenuates α-synuclein aggregation and endoplasmic reticulum stress in rotenone-induced Parkinson's disease rats: A molecular mechanistic study. Biochemical pharmacology 5 38852645
2004 [Protective effects of HRD1 and 4-phenylbutyric acid against neuronal cell death]. Nihon yakurigaku zasshi. Folia pharmacologica Japonica 4 15572843
2006 Cloning and developmental expression of a chick G-protein-coupled receptor SCGPR1. Gene expression patterns : GEP 3 17251065
2004 [Neurodegeneration caused by ER stress?--the pathogenetic mechanisms underlying AR-JP]. Nihon yakurigaku zasshi. Folia pharmacologica Japonica 2 15572841
2014 The Pael-R gene does not mediate the changes in rotenone-induced Parkinson's disease model cells. Neural regeneration research 1 25206827
2007 [Animal models for familial Parkinson's disease]. Rinsho shinkeigaku = Clinical neurology 0 18210841

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