Component
GNAQ (G protein alpha q)
GNAQ (G protein alpha q). Species, exposure and limitations are retained in each linked claim.
2 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.
What it acts on
G-alpha-q increased PLCB3 catalytic turnover in the membrane assay; relief of X-Y-linker autoinhibition was proposed as the mechanism.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/inositol-research/37991948.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fa553185ea3f13a8af7be9a548de14cd13ebe22ff307635fb76675ddc64347d7", "start_char": 0, "end_char": 1735, "text_sha256": "fa553185ea3f13a8af7be9a548de14cd13ebe22ff307635fb76675ddc64347d7"}
- experimental_model
- Reconstituted lipid-bilayer kinetics and membrane-bound structural analysis
- exposure
- G-alpha-q and G-beta-gamma stimulation
- limitations
- Reconstituted biochemical regulation; not an oral inositol intervention. Product generation and lipid depletion occur in the same reaction.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Recombinant mammalian signaling proteins
- plain_language
- A receptor-linked G protein can speed up the enzyme; the detailed allosteric explanation remains an interpretation.
- primary_references
- [ino-p37991948] The mechanism of Gαq regulation of PLCβ3-catalyzed PIP2 hydrolysis. (2023). https://pubmed.ncbi.nlm.nih.gov/37991948/ DOI: 10.1073/pnas.2315011120
- tissue_or_cell_type
- Defined membrane bilayers
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 652–663
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Reconstituted lipid-bilayer kinetics and membrane-bound structural analysis · source_derived_draft · unverified_draft
### ino-gq-plc G-alpha-q increased PLCB3 catalytic turnover in the membrane assay; relief of X-Y-linker autoinhibition was proposed as the mechanism. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: A receptor-linked G protein can speed up the enzyme; the detailed allosteric explanation remains an interpretation. organism: Recombinant mammalian signaling proteins tissue_or_cell_type: Defined membrane bilayers experimental_model: Reconstituted lipid-bilayer kinetics and membrane-bound structural analysis limitations: Reconstituted biochemical regulation; not an oral inositol intervention. Product generation and lipid depletion occur in the same reaction. exposure: G-alpha-q and G-beta-gamma stimulation evidence_span: {"source_cache": "artifacts/inositol-research/37991948.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fa553185ea3f13a8af7be9a548de14cd13ebe22ff307635fb76675ddc64347d7", "start_char": 0, "end_char": 1735, "text_sha256": "fa553185ea3f13a8af7be9a548de14cd13ebe22ff307635fb76675ddc64347d7"} [ino-p37991948] The mechanism of Gαq regulation of PLCβ3-catalyzed PIP2 hydrolysis. (2023). https://pubmed.ncbi.nlm.nih.gov/37991948/ DOI: 10.1073/pnas.2315011120
Complete structured claim and evidence
What acts on it
G-beta-gamma and G-alpha-q could bind PLCB3 simultaneously, with dual stimulation following the product of their independent effects.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/inositol-research/37991948.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fa553185ea3f13a8af7be9a548de14cd13ebe22ff307635fb76675ddc64347d7", "start_char": 0, "end_char": 1735, "text_sha256": "fa553185ea3f13a8af7be9a548de14cd13ebe22ff307635fb76675ddc64347d7"}
- experimental_model
- Reconstituted lipid-bilayer kinetics and membrane-bound structural analysis
- exposure
- G-alpha-q and G-beta-gamma stimulation
- limitations
- Reconstituted biochemical regulation; not an oral inositol intervention. Product generation and lipid depletion occur in the same reaction.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Recombinant mammalian signaling proteins
- plain_language
- Recruiting an enzyme to a membrane and increasing its catalytic rate can cooperate.
- primary_references
- [ino-p37991948] The mechanism of Gαq regulation of PLCβ3-catalyzed PIP2 hydrolysis. (2023). https://pubmed.ncbi.nlm.nih.gov/37991948/ DOI: 10.1073/pnas.2315011120
- tissue_or_cell_type
- Defined membrane bilayers
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 665–676
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Reconstituted lipid-bilayer kinetics and membrane-bound structural analysis · source_derived_draft · unverified_draft
### ino-g-protein-dual G-beta-gamma and G-alpha-q could bind PLCB3 simultaneously, with dual stimulation following the product of their independent effects. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: Recruiting an enzyme to a membrane and increasing its catalytic rate can cooperate. organism: Recombinant mammalian signaling proteins tissue_or_cell_type: Defined membrane bilayers experimental_model: Reconstituted lipid-bilayer kinetics and membrane-bound structural analysis limitations: Reconstituted biochemical regulation; not an oral inositol intervention. Product generation and lipid depletion occur in the same reaction. exposure: G-alpha-q and G-beta-gamma stimulation evidence_span: {"source_cache": "artifacts/inositol-research/37991948.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fa553185ea3f13a8af7be9a548de14cd13ebe22ff307635fb76675ddc64347d7", "start_char": 0, "end_char": 1735, "text_sha256": "fa553185ea3f13a8af7be9a548de14cd13ebe22ff307635fb76675ddc64347d7"} [ino-p37991948] The mechanism of Gαq regulation of PLCβ3-catalyzed PIP2 hydrolysis. (2023). https://pubmed.ncbi.nlm.nih.gov/37991948/ DOI: 10.1073/pnas.2315011120
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.