Affinage

GPR158

Metabotropic glycine receptor · UniProt Q5T848

Length
1215 aa
Mass
135.5 kDa
Annotated
2026-06-10
27 papers in source corpus 18 papers cited in narrative 18 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

GPR158 is a class C orphan GPCR that functions as a synaptic organizing receptor and a master regulator of inhibitory G protein signaling in the brain (PMID:22689652, PMID:28851741). Its intracellular C terminus stabilizes the RGS7-Gβ5 GAP complex post-transcriptionally, maintains its membrane association, and allosterically enhances RGS7 GAP activity, thereby suppressing Gαi/o signaling and cAMP production (PMID:25792749). Cryo-EM structures show GPR158 assembles as a phospholipid-stabilized homodimer with an extracellular Cache/PAS-fold domain and a cytoplasmic coiled-coil that provides a selective docking platform recruiting one or two RGS7-Gβ5 heterodimers (PMID:34793198, PMID:34815401). The extracellular Cache domain directly binds glycine and taurine, defining GPR158 as a metabotropic glycine receptor (mGlyR) whose glycine binding inhibits the associated RGS7-Gβ5 complex and cAMP production to regulate cortical neuronal excitability (PMID:36996198). Downstream, GPR158 controls neuronal excitability by associating with the Kv4.2 channel and suppressing inhibitory cAMP-PKA-mediated phosphorylation (PMID:31311860), and a glycine/GPR158/PKA/ERK/Kv7.2 pathway tunes firing of nucleus accumbens medium spiny neurons (PMID:38884814). At synapses, GPR158 acts as a postsynaptic partner for the heparan sulfate proteoglycan glypican-4 (GPC4) together with the co-receptor LAR to organize mossy fiber-CA3 synapse architecture and presynaptic differentiation (PMID:30290982), and forms a complex with the constitutively active PLCXD2 to restrain PLC activity and control spine apparatus abundance and dendritic spine maturation (PMID:40393451). GPR158 transduces osteocalcin signaling in CA3 neurons to regulate memory and anxiety via IP3 and BDNF (PMID:28851741), and is upregulated by glucocorticoids in the prefrontal cortex where it drives stress-induced depressive-like behavior through effects on AMPA receptor-mediated synaptic strength (PMID:29419376). Beyond its neuronal roles, GPR158 has also been reported to localize to the nucleus via a bipartite NLS and promote cell proliferation in non-neuronal cells (PMID:23451275).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 2012 High

    Established that GPR158 is a binding partner that recruits RGS7 complexes to the membrane and compartmentalizes G protein signaling, answering what cellular function this orphan receptor serves.

    Evidence Reciprocal Co-IP, subcellular fractionation, and a GPR179 night-blindness mouse KO with defined postsynaptic targeting phenotype

    PMID:22689652

    Open questions at the time
    • Did not define the structural basis or the C-terminal element mediating RGS recruitment
    • Endogenous ligand and signaling output unknown
  2. 2015 High

    Mapped the C-terminal determinants by which GPR158 stabilizes RGS7, maintains its membrane association, and allosterically enhances its GAP activity, defining the molecular mechanism of signaling regulation.

    Evidence GPR158 KO mouse, in vitro GAP assays, and C-terminal domain mapping/mutagenesis

    PMID:25792749

    Open questions at the time
    • Atomic structure of the GPR158-RGS7 interface not resolved
    • Upstream activating signal still unknown
  3. 2017 High

    Identified GPR158 as a neuronal receptor for osteocalcin in CA3, linking a peripheral hormone to hippocampal memory and anxiety circuits.

    Evidence KO mice, electrophysiology, behavioral assays, and IP3/BDNF molecular readouts

    PMID:28851741

    Open questions at the time
    • Direct osteocalcin binding to GPR158 not biochemically demonstrated
    • Relationship between OCN signaling and RGS7 GAP activity unclear
  4. 2018 High

    Showed GPR158 is a glucocorticoid-induced driver of stress-induced depression in the PFC acting through synaptic AMPA receptor strength, establishing a behavioral pathophysiological role.

    Evidence Chronic stress model with bidirectional viral overexpression and KO, plus AMPA receptor activity measurements

    PMID:29419376

    Open questions at the time
    • Molecular link between GPR158/RGS7 signaling and AMPA receptor regulation not fully defined
    • Ligand driving GPR158 activity in stress unknown
  5. 2018 High

    Defined GPR158 as a postsynaptic GPC4 binding partner that organizes mossy fiber-CA3 synapse architecture, identifying a trans-synaptic adhesion function distinct from G protein signaling.

    Evidence Reciprocal binding assays, KO mouse, electron microscopy, and electrophysiology

    PMID:30290982

    Open questions at the time
    • How HSPG binding couples to intracellular signaling not resolved at this stage
    • Generalizability beyond mossy fiber-CA3 synapses unknown
  6. 2018 Medium

    Connected GPR158 to a transcriptional feedback loop with RbAp48/Rbbp4 governing memory, implicating it in age-related cognitive decline.

    Evidence Hippocampal RbAp48 inhibition, GPR158 KO, and behavioral memory assays with protein expression analysis

    PMID:30355501

    Open questions at the time
    • Mechanism linking GPR158 signaling to RbAp48 transcription not defined
    • Single lab; feedback loop not independently confirmed
  7. 2019 High

    Demonstrated GPR158 physically associates with Kv4.2 and promotes its function by suppressing cAMP-PKA phosphorylation, defining an effector channel mechanism controlling excitability and depression.

    Evidence Co-IP, patch-clamp electrophysiology, GPR158/RGS7 KO mice, and cAMP-PKA assays

    PMID:31311860

    Open questions at the time
    • Whether GPR158-Kv4.2 association is direct or scaffolded not established
    • Stoichiometry with the RGS7 complex unknown
  8. 2019 Medium

    Showed GPR158 deficiency impairs CA1 dendritic architecture and Schaffer collateral synaptic transmission, broadening its structural role beyond mossy fiber synapses.

    Evidence KO mouse with dendritic morphology analysis, electrophysiology, and spatial memory tests

    PMID:31749686

    Open questions at the time
    • Molecular pathway driving dendritic morphology not defined
    • Single lab
  9. 2021 High

    Resolved cryo-EM structures of GPR158 alone and bound to RGS7-Gβ5, revealing a phospholipid-stabilized homodimer, an extracellular Cache/PAS-fold ligand-binding domain, and the coiled-coil platform underlying selective RGS7 recruitment.

    Evidence Single-particle cryo-EM of apo and RGS7-Gβ5-bound states, independently in two studies

    PMID:34793198 PMID:34815401

    Open questions at the time
    • Endogenous ligand for the Cache domain not identified in these structures
    • Activation/conformational coupling between ligand site and RGS complex unresolved
  10. 2023 High

    Identified glycine and taurine as direct Cache-domain ligands, establishing GPR158 as a metabotropic glycine receptor that inhibits RGS7-Gβ5 signaling and cAMP to control cortical excitability.

    Evidence Cache-domain binding assays, in vitro cAMP signaling, and cortical neuron electrophysiology with KO controls

    PMID:36996198

    Open questions at the time
    • Physiological glycine concentration ranges relevant in vivo not fully mapped
    • Distinct roles of taurine versus glycine downstream incompletely defined
  11. 2024 Medium

    Extended ligand-driven GPR158 signaling to a PKA/ERK/Kv7.2 (M-current) pathway in nucleus accumbens MSNs, linking glycine sensing to a second channel effector.

    Evidence Patch-clamp, PKA/ERK pharmacology, phosphorylation assays, and Kv7 occlusion experiments

    PMID:38884814

    Open questions at the time
    • Direct versus indirect Kv7.2 regulation not resolved
    • Single lab
  12. 2024 Medium

    Showed mPFC GPR158 controls social novelty behavior through excitatory transmission and GluN2B regulation, with rescue establishing causality.

    Evidence Constitutive/conditional KO, viral re-expression, DREADD chemogenetics, western blot, and electron microscopy

    PMID:39383040

    Open questions at the time
    • Mechanistic link from GPR158 signaling to GluN2B phosphorylation not defined
    • Single lab
  13. 2025 Medium

    Defined a GPR158-PLCXD2 postsynaptic complex that restrains constitutive PLC activity to control spine apparatus abundance and spine maturation, revealing a non-canonical receptor-to-PLC pathway gated by HSPG binding.

    Evidence In vivo sparse genetic manipulation, Co-IP, electron microscopy, electrophysiology, and HSPG binding assays

    PMID:40393451

    Open questions at the time
    • How HSPG binding mechanistically modulates the GPR158-PLCXD2 interaction not fully resolved
    • Single lab; PLCXD2 activity regulation by GPR158 not biochemically reconstituted
  14. 2025 Low

    Reported the natural compound trilobatin as a direct GPR158 binder that lowers its expression and links GPR158 to mitophagy and depression, suggesting a pharmacological handle.

    Evidence Direct binding assay, GPR158 KO, CUMS stress model, and mitophagy/autophagy protein readouts

    PMID:39962827

    Open questions at the time
    • Binding site and mechanism of expression reduction not defined
    • Single compound, single lab; mitophagy link not independently confirmed

Open questions

Synthesis pass · forward-looking unresolved questions
  • How ligand binding at the extracellular Cache domain is conformationally transmitted across the dimer to switch the intracellular RGS7-Gβ5 GAP activity, and how this integrates with the adhesion (GPC4) and PLCXD2 effector arms, remains unresolved.
  • No structure capturing a ligand-bound active state coupled to RGS7
  • Integration of glycine sensing, trans-synaptic adhesion, and PLC signaling into one mechanistic model is incomplete

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 3 GO:0098772 molecular function regulator activity 3 GO:0060089 molecular transducer activity 2
Localization
GO:0005886 plasma membrane 3 GO:0005634 nucleus 2
Pathway
R-HSA-112316 Neuronal System 3 R-HSA-162582 Signal Transduction 3
Partners
GNB5GPC4KCND2LARPLCXD2RGS7
Complex memberships
GPR158 homodimerGPR158-PLCXD2 complexGPR158-RGS7-Gβ5 complex

Evidence

Reading pass · 18 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2012 GPR158 (and GPR179) physically interact with RGS7 complexes, recruit them to the plasma membrane, and augment their ability to regulate GPCR signaling; loss of GPR179 in a mouse model of night blindness prevented targeting of RGS to the postsynaptic compartment of bipolar neurons, establishing the functional role of this interaction in compartmentalizing G protein signaling. Co-immunoprecipitation, subcellular fractionation, mouse knockout model (night blindness), plasma membrane recruitment assays The Journal of cell biology High 22689652
2015 GPR158 stabilizes RGS7 post-transcriptionally, maintains its membrane association in the brain, and allosterically enhances RGS7 GTPase-activating protein (GAP) activity through a conserved sequence in the proximal C terminus; the distal C terminus contains PDE-Eγ-like motifs that selectively recruit activated G proteins. Knockout of GPR158 in mice causes marked loss of RGS7 and its membrane association. GPR158 knockout mouse, in vitro GAP activity assays, C-terminal domain mapping/mutagenesis, pulldown assays, western blot The Journal of biological chemistry High 25792749
2017 GPR158 is expressed in neurons of the CA3 region of the hippocampus and transduces osteocalcin (OCN) signaling to regulate hippocampal-dependent memory and anxiety-like behaviors, in part through inositol 1,4,5-trisphosphate (IP3) and BDNF pathways; genetic, electrophysiological, molecular, and behavioral assays established GPR158 as the neuronal receptor for OCN. Genetic (knockout mice), electrophysiology, behavioral assays (memory, anxiety), molecular signaling assays (IP3, BDNF measurement) The Journal of experimental medicine High 28851741
2018 GPR158 is upregulated in the prefrontal cortex (PFC) by glucocorticoids in response to chronic stress; viral overexpression of GPR158 in the PFC induces depressive-like behaviors, while GPR158 ablation produces antidepressant-like phenotype and stress resiliency. GPR158 exerts these effects by modulating synaptic strength via AMPA receptor activity. Chronic stress mouse model, viral overexpression, GPR158 knockout, behavioral assays, glucocorticoid treatment, AMPA receptor activity measurements eLife High 29419376
2018 GPR158 acts as a postsynaptic binding partner for heparan sulfate proteoglycan glypican 4 (GPC4), which is enriched on hippocampal mossy fiber axons; GPR158-induced presynaptic differentiation requires cell-surface GPC4 and co-receptor LAR. Loss of GPR158 increases mossy fiber synapse density but disrupts bouton morphology, active zone and postsynaptic density ultrastructure, and reduces synaptic strength selectively at mossy fiber-CA3 synapses. Co-immunoprecipitation, pulldown assay, immunofluorescence, GPR158 knockout mouse, electron microscopy, electrophysiology Neuron High 30290982
2018 RbAp48/Rbbp4 controls expression of GPR158 and BDNF in the hippocampus; inhibition of RbAp48 inhibits OCN/GPR158-dependent cognition; disruption of OCN/GPR158 signaling downregulates RbAp48, and activation of OCN/GPR158 pathway increases RbAp48 expression in the aged dentate gyrus to rescue age-related memory loss, establishing a feedback loop between RbAp48 and GPR158. Hippocampal RbAp48 inhibition (mouse), GPR158 knockout, behavioral memory assays, western blot for protein expression Cell reports Medium 30355501
2019 GPR158 forms a physical complex with RGS7 that controls A-type potassium channel Kv4.2 subunit in layer 2/3 PFC pyramidal neurons; GPR158 physically associates with Kv4.2 and promotes its function by suppressing inhibitory cAMP-PKA-mediated phosphorylation, thereby controlling neuronal excitability and stress-induced depressive-like behaviors. Co-immunoprecipitation (GPR158-Kv4.2 association), patch-clamp electrophysiology, GPR158/RGS7 knockout mice, chronic stress paradigm, cAMP-PKA assays The Journal of biological chemistry High 31311860
2019 Gpr158 deficiency in mice impairs hippocampal CA1 dendritic architecture (reduced dendritic length, surface, branching in apical but not basal dendrites) and reduces Schaffer collateral-mediated postsynaptic currents while increasing intrinsic excitability of CA1 pyramidal neurons; these morphological deficits correlate with spatial memory impairments. Gpr158 knockout mouse, Morris water maze, passive avoidance test, patch-clamp electrophysiology, dendritic morphology analysis (ex vivo and in vitro) Frontiers in cellular neuroscience Medium 31749686
2021 Cryo-EM structures of human GPR158 alone and in complex with RGS7-Gβ5 reveal: (1) GPR158 forms a homodimer stabilized by a pair of phospholipids; (2) it possesses an extracellular Cache domain as an unusual ligand-binding domain; (3) the structural basis of GPR158 coupling to RGS7-Gβ5 is provided by interaction of the C terminus intracellular coiled-coil region with RGS7. Single-particle cryo-electron microscopy (cryo-EM), structural determination of apo and RGS7-Gβ5-bound states Science (New York, N.Y.) High 34793198
2021 Cryo-EM structures of GPR158 alone and in complex with one or two RGS7-Gβ5 heterodimers reveal: GPR158 dimerizes through Per-Arnt-Sim (PAS)-fold extracellular and TM domains connected by an EGF-like linker; ICL2, ICL3, TM3, and first helix of the cytoplasmic coiled-coil provide a platform for the DHEX domain of one RGS7, while the second helix recruits another RGS7; the unique RGS7-binding site underlies selectivity of GPR158 for RGS7. Cryo-EM structural determination, domain analysis, structure-based selectivity analysis Nature communications High 34815401
2023 GPR158 is a metabotropic glycine receptor (mGlyR): glycine and taurine directly bind to the extracellular Cache domain of GPR158; glycine binding inhibits the RGS7-Gβ5 signaling complex associated with the receptor and inhibits cAMP production; glycine (but not taurine) acts through GPR158 to regulate neuronal excitability in cortical neurons. Ligand binding assays (Cache domain), in vitro signaling assays (cAMP measurement), electrophysiology in cortical neurons, GPR158 knockout comparison Science (New York, N.Y.) High 36996198
2013 In trabecular meshwork cells, glucocorticoid treatment increases GPR158 expression through transcriptional mechanisms; endogenous and overexpressed GPR158 localizes almost entirely to the nucleus via a bipartite nuclear localization signal (NLS) in the 8th helix; inhibition of clathrin-mediated endocytosis shifts GPR158 to the plasma membrane; NLS mutation abrogates GPR158-mediated enhancement of cell proliferation and cyclin D1 upregulation, demonstrating a functional requirement for nuclear localization. siRNA knockdown, transient overexpression, clathrin endocytosis inhibitors, NLS mutagenesis, subcellular fractionation/immunofluorescence, cell proliferation assays, western blot PloS one Medium 23451275
2015 GPR158 promotes prostate cancer cell proliferation independently of androgen receptor (AR) functionality, and this requires nuclear localization; GPR158 expression is stimulated by androgens and GPR158 stimulates AR expression (positive feedback); GPR158 promotes anchorage-independent colony formation and its nuclear localization co-localizes with elevated AR in the Pten knockout mouse prostate tumor model. siRNA knockdown, overexpression, nuclear localization analysis (immunofluorescence), anchorage-independent colony assay, conditional Pten KO mouse model, AR/androgen treatment PloS one Medium 25693195
2019 GPR158 overexpression enhances cAMP production in response to epinephrine in trabecular meshwork cells; Gpr158 knockout mice show altered intraocular pressure response to epinephrine (pressure-lowering effect negated), identifying GPR158 as a homeostatic regulator of intraocular pressure via cAMP signaling. GPR158 overexpression, Gpr158 knockout mouse, cAMP measurement, intraocular pressure measurement, epinephrine challenge Journal of ocular pharmacology and therapeutics Medium 30855200
2024 Glycine-dependent activation of GPR158 in nucleus accumbens medium spiny neurons (MSNs) increases firing rate, reduces M-current (Kv7/KCNQ channels) amplitude, and this effect requires PKA and ERK signaling; GPR158 activation increases ERK phosphorylation and Kv7.2 serine phosphorylation, establishing a GPR158/PKA/ERK/Kv7.2 signaling pathway controlling MSN excitability. Whole-cell patch-clamp recordings, pharmacological inhibitors of PKA and ERK, phosphorylation assays (ERK, Kv7.2), Kv7 channel blockers (occlusion experiments) Cellular and molecular life sciences : CMLS Medium 38884814
2024 GPR158 in pyramidal neurons of the medial PFC controls social novelty behavior; loss of GPR158 reduces excitatory synaptic transmission, glutamate vesicle abundance, and expression/phosphorylation of GluN2B in the mPFC; reintroduction of GPR158 in the mPFC or chemogenetic activation of GPR158-ablated pyramidal neurons rescues the social novelty deficit. Constitutive and conditional Gpr158 knockout, viral GPR158 re-expression, DREADD chemogenetics, behavioral assays, western blot (GluN2B expression/phosphorylation), electron microscopy (glutamate vesicles) Cell reports Medium 39383040
2025 GPR158 forms a postsynaptic complex with PLCXD2 (a constitutively active PLC family member) that controls spine apparatus (SA) abundance in dendritic spines; in the absence of GPR158, unrestrained PLCXD2 activity impedes SA incorporation and hampers structural and functional dendritic spine maturation; extracellular HSPG binding modulates the GPR158-PLCXD2 interaction, providing spatiotemporal control; this establishes a direct GPCR-like receptor-to-PLC signaling pathway bypassing canonical G protein-mediated PLC regulation. Sparse genetic manipulation of mouse cortical neurons in vivo, co-immunoprecipitation (GPR158-PLCXD2), electron microscopy (spine apparatus), electrophysiology, HSPG binding assays Developmental cell Medium 40393451
2025 Trilobatin directly binds to GPR158 and decreases its protein expression level; GPR158 deficiency promotes mitophagy and attenuates depressive-like behaviors; trilobatin's antidepressant effect was strengthened in GPR158-deficient mice, supporting GPR158 as its direct target. Direct binding assay (trilobatin-GPR158), GPR158 knockout mouse, CUMS chronic stress model, mitophagy assays, autophagy-associated protein expression, behavioral assays Journal of agricultural and food chemistry Low 39962827

Source papers

Stage 0 corpus · 27 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2017 Gpr158 mediates osteocalcin's regulation of cognition. The Journal of experimental medicine 240 28851741
2012 GPR158/179 regulate G protein signaling by controlling localization and activity of the RGS7 complexes. The Journal of cell biology 88 22689652
2018 Orphan receptor GPR158 controls stress-induced depression. eLife 67 29419376
2018 RbAp48 Protein Is a Critical Component of GPR158/OCN Signaling and Ameliorates Age-Related Memory Loss. Cell reports 65 30355501
2023 Orphan receptor GPR158 serves as a metabotropic glycine receptor: mGlyR. Science (New York, N.Y.) 58 36996198
2018 An Input-Specific Orphan Receptor GPR158-HSPG Interaction Organizes Hippocampal Mossy Fiber-CA3 Synapses. Neuron 58 30290982
2015 Orphan Receptor GPR158 Is an Allosteric Modulator of RGS7 Catalytic Activity with an Essential Role in Dictating Its Expression and Localization in the Brain. The Journal of biological chemistry 52 25792749
2021 Cryo-EM structure of human GPR158 receptor coupled to the RGS7-Gβ5 signaling complex. Science (New York, N.Y.) 49 34793198
2013 GPR158, an orphan member of G protein-coupled receptor Family C: glucocorticoid-stimulated expression and novel nuclear role. PloS one 43 23451275
2021 Structure of the class C orphan GPCR GPR158 in complex with RGS7-Gβ5. Nature communications 35 34815401
2015 Expression and functional role of orphan receptor GPR158 in prostate cancer growth and progression. PloS one 31 25693195
2018 Inhibition of GPR158 by microRNA-449a suppresses neural lineage of glioma stem/progenitor cells and correlates with higher glioma grades. Oncogene 27 29720725
2019 Gpr158 Deficiency Impacts Hippocampal CA1 Neuronal Excitability, Dendritic Architecture, and Affects Spatial Learning. Frontiers in cellular neuroscience 24 31749686
2019 The signaling proteins GPR158 and RGS7 modulate excitability of L2/3 pyramidal neurons and control A-type potassium channel in the prelimbic cortex. The Journal of biological chemistry 22 31311860
2022 Bevacizumab attenuates osteosarcoma angiogenesis by suppressing MIAT encapsulated by serum-derived extracellular vesicles and facilitating miR-613-mediated GPR158 inhibition. Cell death & disease 17 35347106
2023 Expression Mapping and Functional Analysis of Orphan G-Protein-Coupled Receptor GPR158 in the Adult Mouse Brain Using a GPR158 Transgenic Mouse. Biomolecules 9 36979415
2025 Osteocalcin and GPR158: linking bone and brain function. Frontiers in cell and developmental biology 8 40337551
2024 Glycine-induced activation of GPR158 increases the intrinsic excitability of medium spiny neurons in the nucleus accumbens. Cellular and molecular life sciences : CMLS 8 38884814
2022 The emerging roles of GPR158 in the regulation of the endocrine system. Frontiers in cell and developmental biology 8 36467406
2023 Hyperglycemic microenvironment compromises the homeostasis of communication between the bone-brain axis by the epigenetic repression of the osteocalcin receptor, Gpr158 in the hippocampus. Brain research 6 36634900
2019 GPR158 in the Visual System: Homeostatic Role in Regulation of Intraocular Pressure. Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics 6 30855200
2024 GPR158 in pyramidal neurons mediates social novelty behavior via modulating synaptic transmission in male mice. Cell reports 5 39383040
2025 A postsynaptic GPR158-PLCXD2 complex controls spine apparatus abundance and dendritic spine maturation. Developmental cell 4 40393451
2025 Pharmacological and resting state fMRI reveal Osteocalcin's effects on mouse brain regions with high Gpr37 and Gpr158 expression. Scientific reports 3 40128223
2022 The interaction, mechanism and function of GPR158-RGS7 cross-talk. Progress in molecular biology and translational science 3 36357076
2023 Glycine: a long-sought novel ligand for GPR158. Trends in pharmacological sciences 2 37321907
2025 Trilobatin, a Naturally Occurring GPR158 Ligand, Alleviates Depressive-like Behavior by Promoting Mitophagy. Journal of agricultural and food chemistry 1 39962827

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