Component
Recombinant G-beta5 in the 2023 GPR158 assays
Context-specific entity; species, compartment and exposure are stated on each claim.
1 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
Where it participates (unsigned role)
Glycine slowed G-alpha-o deactivation only when GPR158 was coexpressed with RGS7/G-beta5, supporting inhibition of the complex's GTPase-accelerating activity.
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
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.