Component

Recombinant GPR158 in the 2023 binding/signaling assays

Context-specific entity; species, compartment and exposure are stated on each claim.

4 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

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What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What it acts on

  1. Added glycine reduced cAMP in GPR158-expressing U87 and HEK293 assays; coexpression of RGS7/G-beta5 strengthened the response.

    Recombinant GPR158 in the 2023 binding/signaling assays → cAMP reduction in GPR158-expressing cells source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Recombinant expression and cAMP biosensors.
    limitations
    Direction of cAMP regulation is cell-context dependent; do not infer universal cAMP lowering.
    nutrient_topic
    Glycine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Glycine
    plain_language
    A receptor connects glycine to an intracellular messenger.
    primary_references
    Orphan receptor GPR158 serves as a metabotropic glycine receptor: mGlyR. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36996198/ · DOI 10.1126/science.add7150

    Glycine: supply, one-carbon allocation, receptors and cross-nutrient mechanisms (2026-09-19) · lines 234–240

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Recombinant expression and cAMP biosensors. · source_derived_draft · unverified_draft

    ## glycine-gpr158-camp A receptor connects glycine to an intracellular messenger. Added glycine reduced cAMP in GPR158-expressing U87 and HEK293 assays; coexpression of RGS7/G-beta5 strengthened the response. Model: Recombinant expression and cAMP biosensors. Limitations: Direction of cAMP regulation is cell-context dependent; do not infer universal cAMP lowering. Evidence access: Primary full text Orphan receptor GPR158 serves as a metabotropic glycine receptor: mGlyR. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36996198/ · DOI 10.1126/science.add7150
    Complete structured claim and evidence

What acts on it

  1. Radioligand binding and mutagenesis supported direct glycine recognition by the GPR158 Cache domain, with an estimated binding Kd near 3 micromolar in receptor-expressing membranes.

    Glycine → Recombinant GPR158 in the 2023 binding/signaling assays source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Recombinant GPR158 in HEK293-derived membrane binding assays.
    limitations
    Construct species is not resolved by the accessed main-text methods; human host cells do not establish human receptor sequence. Binding Kd is not an oral dose.
    nutrient_topic
    Glycine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Glycine
    plain_language
    Glycine has a receptor beyond its familiar chloride channel and NMDA site.
    primary_references
    Orphan receptor GPR158 serves as a metabotropic glycine receptor: mGlyR. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36996198/ · DOI 10.1126/science.add7150

    Glycine: supply, one-carbon allocation, receptors and cross-nutrient mechanisms (2026-09-19) · lines 218–224

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Recombinant GPR158 in HEK293-derived membrane binding assays. · source_derived_draft · unverified_draft

    ## glycine-gpr158-binding Glycine has a receptor beyond its familiar chloride channel and NMDA site. Radioligand binding and mutagenesis supported direct glycine recognition by the GPR158 Cache domain, with an estimated binding Kd near 3 micromolar in receptor-expressing membranes. Model: Recombinant GPR158 in HEK293-derived membrane binding assays. Limitations: Construct species is not resolved by the accessed main-text methods; human host cells do not establish human receptor sequence. Binding Kd is not an oral dose. Evidence access: Primary full text Orphan receptor GPR158 serves as a metabotropic glycine receptor: mGlyR. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36996198/ · DOI 10.1126/science.add7150
    Complete structured claim and evidence

  2. Taurine competed for GPR158 glycine binding and produced weaker cAMP suppression than glycine in the recombinant assays.

    Taurine → Recombinant GPR158 in the 2023 binding/signaling assays source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Membrane ligand competition and cell signaling.
    limitations
    Shared binding is not proof of supplement synergy or the same neuronal response.
    nutrient_topic
    Glycine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Glycine
    plain_language
    Another nutrient-related molecule reaches the same receptor with a different response.
    primary_references
    Orphan receptor GPR158 serves as a metabotropic glycine receptor: mGlyR. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36996198/ · DOI 10.1126/science.add7150

    Glycine: supply, one-carbon allocation, receptors and cross-nutrient mechanisms (2026-09-19) · lines 242–248

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Membrane ligand competition and cell signaling. · source_derived_draft · unverified_draft

    ## glycine-gpr158-taurine Another nutrient-related molecule reaches the same receptor with a different response. Taurine competed for GPR158 glycine binding and produced weaker cAMP suppression than glycine in the recombinant assays. Model: Membrane ligand competition and cell signaling. Limitations: Shared binding is not proof of supplement synergy or the same neuronal response. Evidence access: Primary full text Orphan receptor GPR158 serves as a metabotropic glycine receptor: mGlyR. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36996198/ · DOI 10.1126/science.add7150
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Glycine slowed G-alpha-o deactivation only when GPR158 was coexpressed with RGS7/G-beta5, supporting inhibition of the complex's GTPase-accelerating activity.

    Glycine → GPR158-associated RGS7/G-beta5 assay complex source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Recombinant cellular BRET assays, including 100 micromolar glycine comparisons.
    limitations
    Functional coupling does not prove every intervening conformational step or a clinical mood effect.
    nutrient_topic
    Glycine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Glycine
    plain_language
    Receptor binding changes how quickly another signaling switch is turned off.
    primary_references
    Orphan receptor GPR158 serves as a metabotropic glycine receptor: mGlyR. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36996198/ · DOI 10.1126/science.add7150

    Glycine: supply, one-carbon allocation, receptors and cross-nutrient mechanisms (2026-09-19) · lines 226–232

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Recombinant cellular BRET assays, including 100 micromolar glycine comparisons. · source_derived_draft · unverified_draft

    ## glycine-gpr158-rgs-inhibition Receptor binding changes how quickly another signaling switch is turned off. Glycine slowed G-alpha-o deactivation only when GPR158 was coexpressed with RGS7/G-beta5, supporting inhibition of the complex's GTPase-accelerating activity. Model: Recombinant cellular BRET assays, including 100 micromolar glycine comparisons. Limitations: Functional coupling does not prove every intervening conformational step or a clinical mood effect. Evidence access: Primary full text Orphan receptor GPR158 serves as a metabotropic glycine receptor: mGlyR. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36996198/ · DOI 10.1126/science.add7150
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

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