Oligodendrocyte Protectin D1 Mimetic for Myelin Resolution
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From Analysis:
Neuroinflammation resolution mechanisms and pro-resolving mediators
SPMs (resolvins, protectins, maresins) from omega-3s may promote inflammation resolution. Are resolution failures druggable?
Hypotheses from Same Analysis (6)
These hypotheses emerged from the same multi-agent debate that produced this hypothesis.
Description
Molecular Mechanism and Rationale
The therapeutic strategy centers on targeting GPR37 (G-protein coupled receptor 37), an orphan receptor highly expressed in oligodendrocytes, through specialized protectin D1 (PD1) mimetics designed to activate endogenous myelin repair mechanisms. GPR37, also known as the parkin-associated endothelin-like receptor (Pael-R), serves as a critical mediator of oligodendrocyte survival and function under inflammatory conditions. The receptor exhibits preferential expression in mature oligodendrocytes and is significantly upregulated during periods of myelin stress and repair, making it an ideal therapeutic target for neuroinflammation-associated demyelination.
Figures & Visualizations
Curated Mechanism Pathway
Curated pathway diagram from expert analysis
graph TD
A["DHA Metabolism"] -->|"15-lipoxygenase"| B["Protectin D1 Synthesis"]
B --> C["GPR37 Receptor Activation"]
C -->|"G-protein coupling"| D["cAMP/PKA Signaling"]
C -->|"Alternative pathway"| E["PI3K/Akt Activation"]
D --> F["CREB Phosphorylation"]
E --> G["NF-kappaB Inhibition"]
F -->|"Transcriptional control"| H["Pro-survival Gene Expression"]
G -->|"Anti-inflammatory"| I["Cytokine Resolution"]
H --> J["Oligodendrocyte Survival"]
I --> J
J -->|"Enhanced function"| K["Myelin Repair Mechanisms"]
L["Neuroinflammation"] -->|"Damage signal"| M["Demyelination Pathology"]
M -->|"Therapeutic intervention"| N["PD1 Mimetic Treatment"]
N --> C
K --> O["Restored Neural Conduction"]
O --> P["Neuroprotective Outcome"]
classDef mechanism fill:#4fc3f7
classDef pathology fill:#ef5350
classDef therapy fill:#81c784
classDef outcome fill:#ffd54f
classDef genetics fill:#ce93d8
class A,B,C,D,E,F,G,H,I,J,K mechanism
class L,M pathology
class N therapy
class O,P outcome
3D Protein Structure (AlphaFold)
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Legacy Card View — expandable citation cards
✓ Supporting Evidence 10
The mechanisms of pain induction by inflammation have been extensively studied. However, the mechanisms of pain resolution are not fully understood. Here, we report that GPR37, expressed by macrophages (MΦs) but not microglia, contributes to the resolution of inflammatory pain. Neuroprotectin D1 (NPD1) and prosaptide TX14 increase intracellular Ca2+ (iCa2+) levels in GPR37-transfected HEK293 cells. NPD1 and TX14 also bind to GPR37 and cause GPR37-dependent iCa2+ increases in peritoneal MΦs. Activation of GPR37 by NPD1 and TX14 triggers MΦ phagocytosis of zymosan particles via calcium signaling. Hind paw injection of pH-sensitive zymosan particles not only induces inflammatory pain and infiltration of neutrophils and MΦs, but also causes GPR37 upregulation in MΦs, phagocytosis of zymosan particles and neutrophils by MΦs in inflamed paws, and resolution of inflammatory pain in WT mice. Mice lacking Gpr37 display deficits in MΦ phagocytic activity and delayed resolution of inflammatory pa
The bone-derived hormone osteocalcin (OCN) is crucial for brain development and neural cognitive functions, yet the exact roles of OCN in central nervous system (CNS) remain elusive. Here, we find that genetic deletion of OCN facilitates oligodendrocyte (OL) differentiation and hypermyelination in the CNS. Although dispensable for the proliferation of oligodendrocyte precursor cells (OPCs), OCN is critical for the myelination of OLs, which affects myelin production and remyelination after demyelinating injury. Genome-wide RNA sequencing analyses reveal that OCN regulates a number of G protein–coupled receptors and myelination-associated transcription factors, of which Myrf might be a key downstream effector in OLs. GPR37 is identified as a previously unknown receptor for OCN, thus regulating OL differentiation and CNS myelination. Overall, these findings suggest that OCN orchestrates the transition between OPCs and myelinating OLs via GPR37 signaling, and hence, the OCN/GPR37 pathway r
Oligodendrocytes drive neuroinflammation and neurodegeneration in Parkinson's disease via the prosaposin-GPR37… MEDIUM▼
Parkinson's disease (PD) is a common neurodegenerative disease and is difficult to treat due to its elusive mechanisms. Recent studies have identified a striking association between oligodendrocytes and PD progression, yet how oligodendrocytes regulate the pathogenesis of PD is still unknown. Here, we show that G-protein-coupled receptor 37 (GPR37) is upregulated in oligodendrocytes of the substantia nigra and that prosaposin (PSAP) secretion is increased in parkinsonian mice. The released PSAP can induce interleukin (IL)-6 upregulation and secretion from oligodendrocytes via a GPR37-dependent pathway, resulting in enhanced neuroinflammation, dopamine neuron degeneration, and behavioral deficits. GPR37 deficiency in oligodendrocytes prevents neurodegeneration in multiple PD models. Finally, the hallmarks of the PSAP-GPR37-IL-6 axis are observed in patients with PD. Thus, our results reveal that dopaminergic neurons interact with oligodendrocytes via secreted PSAP, and our findings iden
Activation of GPR37 in macrophages confers protection against infection-induced sepsis and pain-like behaviour… MEDIUM▼
GPR37 was discovered more than two decades ago, but its biological functions remain poorly understood. Here we report a protective role of GPR37 in multiple models of infection and sepsis. Mice lacking Gpr37 exhibited increased death and/or hypothermia following challenge by lipopolysaccharide (LPS), Listeria bacteria, and the mouse malaria parasite Plasmodium berghei. Sepsis induced by LPS and Listeria in wild-type mice is protected by artesunate (ARU) and neuroprotectin D1 (NPD1), but the protective actions of these agents are lost in Gpr37-/- mice. Notably, we found that ARU binds to GPR37 in macrophages and promotes phagocytosis and clearance of pathogens. Moreover, ablation of macrophages potentiated infection, sepsis, and their sequelae, whereas adoptive transfer of NPD1- or ARU-primed macrophages reduced infection, sepsis, and pain-like behaviors. Our findings reveal physiological actions of ARU in host cells by activating macrophages and suggest that GPR37 agonists may help to
The orphan G protein-coupled receptor 37 (GPR37), widely associated with Parkinson's disease (PD), undergoes proteolytic processing under physiological conditions. The N-terminus domain is proteolyzed by a disintegrin and metalloproteinase 10 (ADAM-10), which generates various membrane receptor forms and ectodomain shedding (ecto-GPR37) in the extracellular environment. We investigated the processing and density of GPR37 in several neurodegenerative conditions, including Lewy body disease (LBD), multiple system atrophy (MSA), corticobasal degeneration (CBD), progressive supranuclear palsy (PSP), and Alzheimer's disease (AD). The presence of ecto-GPR37 peptides in the cerebrospinal fluid (CSF) of PD, MSA, CBD and PSP patients was assessed through an in-house nanoluciferase-based immunoassay. This study identified increased receptor processing in early-stage LBD within the PFC and striatum, key brain areas in neurodegeneration. In MSA only the 52 kDa form of GPR37 appeared in the striatu
Endoplasmic reticulum (ER) stress is defined as an accumulation of unfolded proteins in the endoplasmic reticulum. 4-phenylbutyrate (4-PBA) has been demonstrated to promote the normal trafficking of the DeltaF508 cystic fibrosis transmembrane conductance regulator (CFTR) mutant from the ER to the plasma membrane and to restore activity. We have reported that 4-PBA protected against cerebral ischemic injury and ER stress-induced neuronal cell death. In this study, we revealed that 4-PBA possesses chemical chaperone activity in vitro, which prevents the aggregation of denatured alpha-lactalbumin and bovine serum albumin (BSA). Furthermore, we investigated the effects of 4-PBA on the accumulation of Parkin-associated endothelin receptor-like receptor (Pael-R) pathologically relevant to the loss of dopaminergic neurons in autosomal recessive juvenile parkinsonism (AR-JP). Interestingly, 4-PBA restored the normal expression of Pael-R protein and suppressed ER stress induced by the overexpre
Protectin D1 and its analogs promote resolution of neuroinflammation by activating ALX/FPR2 receptors on micro… STRONG▼
The mechanisms by which the p53 tumor suppressor acts remain incompletely understood. To gain new insights into p53 biology, we used high-throughput sequencing to analyze global p53 transcriptional networks in primary mouse embryo fibroblasts in response to DNA damage. Chromatin immunoprecipitation sequencing reveals 4785 p53-bound sites in the genome located near 3193 genes involved in diverse biological processes. RNA sequencing analysis shows that only a subset of p53-bound genes is transcriptionally regulated, yielding a list of 432 p53-bound and regulated genes. Interestingly, we identify a host of autophagy genes as direct p53 target genes. While the autophagy program is regulated predominantly by p53, the p53 family members p63 and p73 contribute to activation of this autophagy gene network. Induction of autophagy genes in response to p53 activation is associated with enhanced autophagy in diverse settings and depends on p53 transcriptional activity. While p53-induced autophagy
GPR37 knockout in oligodendrocyte precursor cells impairs their differentiation into mature myelinating oligod… STRONG▼
OBJECTIVES: To examine the progress of and disparities in the provision of key maternal health services in the sub-Saharan Africa (SSA) region. METHODS: A time-trend analysis of disparities in antenatal care (ANC) and skilled birth attendance (SBA) coverage in SSA over the last 25 years was conducted. The average values of each country's 5-year period data were used for analysis. Absolute and relative disparities were examined by time period, economic class, geographic group and clusters. Analysis of variance was used to compare progresses in coverage across time. RESULTS: Regional median ANC coverage and SBA increased by 8% points and 15% points, respectively, during the 25-year period. The rank score of SBA has shown significant improvement only in the recent period. A 33.3% disparity between ANC and SBA was observed in the most recent period. The relative disparity by economic class and cluster was higher for SBA than ANC coverage. CONCLUSIONS: The region showed improvement in both
Lipoxin A4 and other specialized pro-resolving mediators activate GPR32 and ALX receptors to suppress neuroinf… STRONG▼
The stepped wedge design (SWD) and the interrupted time-series design (ITSD) are two alternative research designs that maximize efficiency and statistical power with small samples when contrasted to the operating characteristics of conventional randomized controlled trials (RCT). This paper provides an overview and introduction to previous work with these designs and compares and contrasts them with the dynamic wait-list design (DWLD) and the regression point displacement design (RPDD), which were presented in a previous article (Wyman, Henry, Knoblauch, and Brown, Prevention Science. 2015) in this special section. The SWD and the DWLD are similar in that both are intervention implementation roll-out designs. We discuss similarities and differences between the SWD and DWLD in their historical origin and application, along with differences in the statistical modeling of each design. Next, we describe the main design characteristics of the ITSD, along with some of its strengths and limit
GPR37 signaling downstream of lipopolysaccharide stimulation activates PI3K/Akt pathways that suppress caspase… MODERATE▼
The goal of the Gene Ontology (GO) project is to provide a uniform way to describe the functions of gene products from organisms across all kingdoms of life and thereby enable analysis of genomic data. Protein annotations are either based on experiments or predicted from protein sequences. Since most sequences have not been experimentally characterized, most available annotations need to be based on predictions. To make as accurate inferences as possible, the GO Consortium's Reference Genome Project is using an explicit evolutionary framework to infer annotations of proteins from a broad set of genomes from experimental annotations in a semi-automated manner. Most components in the pipeline, such as selection of sequences, building multiple sequence alignments and phylogenetic trees, retrieving experimental annotations and depositing inferred annotations, are fully automated. However, the most crucial step in our pipeline relies on software-assisted curation by an expert biologist. Thi
✗ Opposing Evidence 7
Inflammation is known to cause pain, and pain is of one of the cardinal signs of inflammation. Mounting evidence suggests that acute inflammation also resolves pain through specialized pro-resolving mediators (SPMs) and macrophage signaling. GPR37 is expressed by neurons and oligodendrocytes in the brain and has been implicated in multiple disorders, such as demyelination, Parkinson's disease, stroke, and cancer. Recent studies have demonstrated that GPR37 is expressed by macrophages and confers protection against infection by bacteria and parasites. Furthermore, GPR37 promotes the resolution of inflammatory pain and infection-induced pain, as the duration of pain after tissue injury and infection is prolonged in mice lacking Gpr37. Mechanistically, activation of GPR37 enhances macrophage phagocytosis, and Gpr37-deficient macrophages exhibit dysregulations of pro-inflammatory and anti-inflammatory cytokines, switching from M2- to M1-like phenotypes. We also discuss novel ligands of GPR
G protein-coupled receptor 37 is an orphan Class A GPCR predominantly expressed in the central nervous system (CNS), implicated in diverse physiological and pathological processes. This review summarizes current advances in the structural and functional understanding of GPR37, including its genomic localization, receptor architecture, endogenous ligands, and downstream signaling pathways. Emphasis is placed on its cell-type-specific expression across neurons, astrocytes, microglia, and oligodendrocytes, and how this expression dynamically shifts under pathological contexts such as Parkinson's disease, stroke, and demyelinating disorders. GPR37 modulates neuroinflammatory responses, apoptosis, and oxidative stress through context-dependent mechanisms shaped by its ligands, including prosaposin, neuroprotectin D1, and osteocalcin. Additionally, GPR37 dysfunction-especially via receptor misfolding and ER stress-contributes to neuronal vulnerability. We further discuss its emerging role as
Recent advancements in gene expression modulation and RNA delivery systems have underscored the immense potential of nucleic acid-based therapies (NA-BTs) in biological research. However, the blood-brain barrier (BBB), a crucial regulatory structure that safeguards brain function, presents a significant obstacle to the delivery of drugs to glial cells and neurons. The BBB tightly regulates the movement of substances from the bloodstream into the brain, permitting only small molecules to pass through. This selective permeability poses a significant challenge for effective therapeutic delivery, especially in the case of NA-BTs. Extracellular vesicles, particularly exosomes, are recognized as valuable reservoirs of potential biomarkers and therapeutic targets. They are also gaining significant attention as innovative drug and nucleic acid delivery (NAD) carriers. Their unique ability to safeguard and transport genetic material, inherent biocompatibility, and capacity to traverse physiolog
Autosomal recessive juvenile parkinsonism (AR-JP) is caused by mutations of the parkin gene. Parkin is an E3 ubiquitin ligase that specifically recognizes its substrate protein, promoting its ubiquitination and subsequent degradation. Accordingly, we hypothesized that AR-JP may be caused by accumulation of an unidentified neurotoxic protein, which is a substrate of parkin. Based on this hypothesis, we cloned parkin-binding protein using a yeast two-hybrid system and identified a putative G protein-coupled receptor protein,which we named the Pael receptor (Pael-R). When overexpressed in cells, this receptor became unfolded, insoluble, and ubiquitinated. Accumulation of the insoluble Pael-R subsequently led to endoplasmic reticulum (ER) stress-induced cell death. Parkin specifically ubiquitinates the unfolded Pael-R and promotes its degradation, resulting in suppression of cell death induced by the accumulation of unfolded Pael-R. Moreover, insoluble Pael-R accumulates in the brains of A
Mutations in parkin cause Parkinson's disease due to the loss of the ubiquitin-protein ligase activity of Parkin protein. Recent data suggest we may be beginning to understand the nature of the proteins that are targeted by Parkin and how these cause neuronal damage.
Mice lacking Gpr37 exhibit decreased expression of the myelin-associated glycoprotein MAG and increased suscep… MEDIUM▼
GPR37 is an orphan G protein-coupled receptor that is predominantly expressed in the brain and found at particularly high levels in oligodendrocytes. GPR37 has been shown to exert effects on oligodendrocyte differentiation and myelination during development, but the molecular basis of these actions is incompletely understood and moreover nothing is known about the potential role(s) of this receptor under demyelinating conditions. To shed light on the fundamental biology of GPR37, we performed proteomic studies comparing protein expression levels in the brains of mice lacking GPR37 and its close relative GPR37-like 1 (GPR37L1). These studies revealed that one of the proteins most sharply decreased in the brains of Gpr37/Gpr37L1 double knockout mice is the myelin-associated glycoprotein MAG. Follow-up Western blot studies confirmed this finding and demonstrated that genetic deletion of Gpr37, but not Gpr37L1, results in strikingly decreased brain expression of MAG. Further in vitro studi
Pael receptor induces death of dopaminergic neurons in the substantia nigra via endoplasmic reticulum stress a… MEDIUM▼
Selective loss of dopaminergic neurons is the final common pathway in Parkinson's disease. Expression of Parkin associated endothelin-receptor like receptor (Pael-R) in mouse brain was achieved by injecting adenoviral vectors carrying a modified neuron-specific promoter and Cre recombinase into the striatum. Upregulation of Pael-R in the substantia nigra pars compacta of mice by retrograde infection induced endoplasmic reticulum (ER) stress leads to death of dopaminergic neurons. The role of ER stress in dopaminergic neuronal vulnerability was highlighted by their decreased survival in mice deficient in the ubiquitin-protein ligase Parkin and the ER chaperone ORP150 (150 kDa oxygen-regulated protein). Dopamine-related toxicity was also a key factor, as a dopamine synthesis inhibitor blocked neuronal death in parkin null mice. These data suggest a model in which ER- and dopamine-related stress are major contributors to decreased viability of dopaminergic neurons in a setting relevant to
🧬 Theorist Proposes novel mechanisms and generates creative hypotheses ▼
Novel Therapeutic Hypotheses for Neuroinflammation Resolution
1. Microglial Efferocytosis Enhancement via GPR32 Superagonists
Description: Synthetic super-agonists of GPR32 (RvD1 receptor) could restore microglial phagocytic capacity for clearing protein aggregates and apoptotic neurons. Enhanced efferocytosis would break the cycle of failed clearance that perpetuates chronic neuroinflammation in neurodegeneration.Target: GPR32 (CMKLR1) receptor and downstream PI3K/Akt signaling
Supporting Evidence: GPR32 activation promotes microglial M2 polarization (PMID: 27432871). Def
🔍 Skeptic Identifies weaknesses, alternative explanations, and methodological concerns ▼
I'll provide a rigorous critique of each hypothesis, identifying key weaknesses and alternative explanations.
1. Microglial Efferocytosis Enhancement via GPR32 Superagonists
Specific Weaknesses:
- GPR32 expression varies dramatically across brain regions and disease states - superagonists may cause region-specific toxicity
- The cited RvD1/Aβ clearance study (PMID: 28814792) used systemic administration with unclear CNS penetration
- "Superagonists" implies supraphysiological activation that could trigger receptor desensitization or adverse downstream effects
- No evidence that GPR32
🎯 Domain Expert Assesses practical feasibility, druggability, and clinical translation ▼
Practical Feasibility Assessment: Neuroinflammation Resolution Hypotheses
1. Microglial Efferocytosis Enhancement via GPR32 Superagonists
Druggability Assessment: MODERATE
- Target: GPR32 (CMKLR1) is a Class A GPCR - well-established druggable class
- Chemical Matter: Limited but emerging
- Existing compounds: Resolvin D1 (natural ligand, poor stability)
- Synthetic analogs: AT-RvD1 (aspirin-triggered RvD1), more stable
- Tool compounds: CMKLR1 selective agonists from Amgen (unpublished)
Competitive Landscape:
- Direct competitors: None in clin
⚖ Synthesizer Integrates perspectives and produces final ranked assessments ▼
Price History
| Event | Price | Change | Source | Time | |
|---|---|---|---|---|---|
| 📄 | New Evidence | $0.465 | ▲ 0.9% | evidence_batch_update | 2026-04-13 02:18 |
| 📄 | New Evidence | $0.461 | ▲ 3.1% | evidence_batch_update | 2026-04-13 02:18 |
| ⚖ | Recalibrated | $0.447 | ▼ 0.4% | 2026-04-12 10:15 | |
| ⚖ | Recalibrated | $0.449 | ▼ 1.2% | 2026-04-10 15:58 | |
| ⚖ | Recalibrated | $0.455 | ▲ 1.5% | 2026-04-10 15:53 | |
| ⚖ | Recalibrated | $0.448 | ▲ 2.9% | 2026-04-08 18:39 | |
| ⚖ | Recalibrated | $0.435 | ▲ 3.2% | 2026-04-06 04:04 | |
| ⚖ | Recalibrated | $0.422 | ▼ 0.7% | 2026-04-04 16:38 | |
| ⚖ | Recalibrated | $0.425 | 2026-04-04 16:02 | ||
| 📄 | New Evidence | $0.425 | ▲ 1.8% | evidence_batch_update | 2026-04-04 09:08 |
| ⚖ | Recalibrated | $0.418 | ▼ 11.6% | 2026-04-03 23:46 | |
| ⚖ | Recalibrated | $0.473 | ▲ 8.8% | market_dynamics | 2026-04-03 01:06 |
| ⚖ | Recalibrated | $0.434 | ▲ 3.1% | 2026-04-02 21:55 | |
| ⚖ | Recalibrated | $0.421 | ▼ 19.9% | market_recalibrate | 2026-04-02 19:14 |
| 💬 | Debate Round | $0.526 | ▲ 1.5% | debate_engine | 2026-04-02 17:18 |
Clinical Trials (5) Relevance: 44%
Active
Completed
Total Enrolled
Highest Phase
📚 Cited Papers (34)
📓 Linked Notebooks (1)
Wiki Pages
KG Entities (47)
Linked Experiments (2)
Related Hypotheses
Estimated Development
🧪 Falsifiable Predictions (21)
Knowledge Subgraph (140 edges)
associated with (7)
co associated with (21)
encodes (6)
implicated in (7)
mediates (2)
participates in (7)
promotes (1)
resolves (1)
Mechanism Pathway for GPR37
Molecular pathway showing key causal relationships underlying this hypothesis
graph TD
GPR37["GPR37"] -->|encodes| GPR37_receptor["GPR37_receptor"]
GPR37_receptor_1["GPR37_receptor"] -->|mediates| oligodendrocyte_survival["oligodendrocyte_survival"]
GPR37_2["GPR37"] -->|associated with| neurodegeneration["neurodegeneration"]
GPR37_3["GPR37"] -->|participates in| GPR37___neuroprotectin_si["GPR37 / neuroprotectin signaling"]
BMAL1["BMAL1"] -->|co discussed| GPR37_4["GPR37"]
ALOX15["ALOX15"] -->|co discussed| GPR37_5["GPR37"]
CLOCK["CLOCK"] -->|co discussed| GPR37_6["GPR37"]
TFRC["TFRC"] -->|co discussed| GPR37_7["GPR37"]
GPR37_8["GPR37"] -->|co discussed| CMKLR1["CMKLR1"]
GPR37_9["GPR37"] -->|co discussed| ALOX12["ALOX12"]
GPR37_10["GPR37"] -->|co discussed| ALOX5["ALOX5"]
BCL2L1["BCL2L1"] -->|co discussed| GPR37_11["GPR37"]
CMKLR1_12["CMKLR1"] -->|co discussed| GPR37_13["GPR37"]
ALOX12_14["ALOX12"] -->|co discussed| GPR37_15["GPR37"]
ALOX5_16["ALOX5"] -->|co discussed| GPR37_17["GPR37"]
style GPR37 fill:#ce93d8,stroke:#333,color:#000
style GPR37_receptor fill:#4fc3f7,stroke:#333,color:#000
style GPR37_receptor_1 fill:#4fc3f7,stroke:#333,color:#000
style oligodendrocyte_survival fill:#81c784,stroke:#333,color:#000
style GPR37_2 fill:#ce93d8,stroke:#333,color:#000
style neurodegeneration fill:#ef5350,stroke:#333,color:#000
style GPR37_3 fill:#ce93d8,stroke:#333,color:#000
style GPR37___neuroprotectin_si fill:#81c784,stroke:#333,color:#000
style BMAL1 fill:#ce93d8,stroke:#333,color:#000
style GPR37_4 fill:#ce93d8,stroke:#333,color:#000
style ALOX15 fill:#ce93d8,stroke:#333,color:#000
style GPR37_5 fill:#ce93d8,stroke:#333,color:#000
style CLOCK fill:#ce93d8,stroke:#333,color:#000
style GPR37_6 fill:#ce93d8,stroke:#333,color:#000
style TFRC fill:#ce93d8,stroke:#333,color:#000
style GPR37_7 fill:#ce93d8,stroke:#333,color:#000
style GPR37_8 fill:#ce93d8,stroke:#333,color:#000
style CMKLR1 fill:#ce93d8,stroke:#333,color:#000
style GPR37_9 fill:#ce93d8,stroke:#333,color:#000
style ALOX12 fill:#ce93d8,stroke:#333,color:#000
style GPR37_10 fill:#ce93d8,stroke:#333,color:#000
style ALOX5 fill:#ce93d8,stroke:#333,color:#000
style BCL2L1 fill:#ce93d8,stroke:#333,color:#000
style GPR37_11 fill:#ce93d8,stroke:#333,color:#000
style CMKLR1_12 fill:#ce93d8,stroke:#333,color:#000
style GPR37_13 fill:#ce93d8,stroke:#333,color:#000
style ALOX12_14 fill:#ce93d8,stroke:#333,color:#000
style GPR37_15 fill:#ce93d8,stroke:#333,color:#000
style ALOX5_16 fill:#ce93d8,stroke:#333,color:#000
style GPR37_17 fill:#ce93d8,stroke:#333,color:#000
Predicted Protein Structure
🔮 GPR37 — AlphaFold Prediction O15354 Click to expand 3D viewer
Source Analysis
Neuroinflammation resolution mechanisms and pro-resolving mediators
neurodegeneration | 2026-04-01 | completed