Component

DAG

Acyl-linked glycerol substrate for diacyl phosphatidylethanolamine synthesis.

10 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.

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.

Recorded relationships

What acts on it

  1. Diacylglycerol was the lipid product of PLCB3-catalyzed PI(4,5)P2 hydrolysis.

    PLCB3 (phospholipase C beta 3) → DAG source_derived_draftungraded
    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
    The second product stays in the membrane rather than becoming soluble IP3.
    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 639–650

    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-plc-dag Diacylglycerol was the lipid product of PLCB3-catalyzed PI(4,5)P2 hydrolysis. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: The second product stays in the membrane rather than becoming soluble IP3. 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

Where it participates (unsigned role)

  1. Human CHPT1 catalyzes the PC-producing final step of the Kennedy pathway with choline-headgroup substrate selectivity.

    Human choline phosphotransferase 1 / CHPT1 → Phosphatidylcholine source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/choline-research/40435706.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d08b2ce68e8731e88e1204dc1b09d1301020452752a630a880ec3a2cdb0f2351", "start_char": 0, "end_char": 1339, "text_sha256": "d08b2ce68e8731e88e1204dc1b09d1301020452752a630a880ec3a2cdb0f2351"}
    experimental_model
    Human CHPT1 cryo-EM, sequence analysis and biochemical characterization
    exposure
    CDP-choline/CDP-ethanolamine substrate selectivity
    limitations
    Human CHPT1 and CEPT1 remain separate. Evolutionary suggestions about oviparous species are not asserted as human bifunctionality.
    nutrient_topic
    Choline research collection; topical membership is not evidence of a direct dietary effect. · Choline
    organism
    Human proteins; evolutionary comparisons explicitly separate
    plain_language
    One terminal enzyme specializes in making phosphatidylcholine.
    primary_references
    [choline-p40435706] Structural basis for substrate selectivity and evolutionary insights into human choline phosphotransferase 1. (2025). https://pubmed.ncbi.nlm.nih.gov/40435706/ DOI: 10.1016/j.bbrc.2025.152082
    tissue_or_cell_type
    Membrane phospholipid synthesis

    Choline: metabolism, signaling and nutrient connections (2026-09-17) · lines 763–774

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human CHPT1 cryo-EM, sequence analysis and biochemical characterization · source_derived_draft · unverified_draft

    ### choline-chpt1-pc Human CHPT1 catalyzes the PC-producing final step of the Kennedy pathway with choline-headgroup substrate selectivity. Condition category: normal nutrient_topic: Choline research collection; topical membership is not evidence of a direct dietary effect. plain_language: One terminal enzyme specializes in making phosphatidylcholine. organism: Human proteins; evolutionary comparisons explicitly separate tissue_or_cell_type: Membrane phospholipid synthesis experimental_model: Human CHPT1 cryo-EM, sequence analysis and biochemical characterization limitations: Human CHPT1 and CEPT1 remain separate. Evolutionary suggestions about oviparous species are not asserted as human bifunctionality. exposure: CDP-choline/CDP-ethanolamine substrate selectivity evidence_span: {"source_cache": "artifacts/choline-research/40435706.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d08b2ce68e8731e88e1204dc1b09d1301020452752a630a880ec3a2cdb0f2351", "start_char": 0, "end_char": 1339, "text_sha256": "d08b2ce68e8731e88e1204dc1b09d1301020452752a630a880ec3a2cdb0f2351"} [choline-p40435706] Structural basis for substrate selectivity and evolutionary insights into human choline phosphotransferase 1. (2025). https://pubmed.ncbi.nlm.nih.gov/40435706/ DOI: 10.1016/j.bbrc.2025.152082
    Complete structured claim and evidence

  2. Benfotiamine inhibited AGE-pathway activation in the experimental hyperglycemia models.

    Benfotiamine → Advanced glycation end-product formation source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    High-glucose bovine endothelial cells and diabetic rat retinal experiments.
    exposure
    Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine.
    limitations
    Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Bos taurus; Rattus norvegicus
    plain_language
    Less activation of a glycation pathway accompanied the intervention.
    primary_references
    [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
    tissue_or_cell_type
    Endothelial cultures and retina

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1903–1913

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High-glucose bovine endothelial cells and diabetic rat retinal experiments. · source_derived_draft · unverified_draft

    ### b1-benfotiamine-age Benfotiamine inhibited AGE-pathway activation in the experimental hyperglycemia models. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Less activation of a glycation pathway accompanied the intervention. organism: Bos taurus; Rattus norvegicus tissue_or_cell_type: Endothelial cultures and retina experimental_model: High-glucose bovine endothelial cells and diabetic rat retinal experiments. limitations: Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase. exposure: Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine. [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
    Complete structured claim and evidence

  3. Benfotiamine inhibited hyperglycemia-associated hexosamine-pathway activation in the tested models.

    Benfotiamine → Hexosamine pathway activity source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    High-glucose bovine endothelial cells and diabetic rat retinal experiments.
    exposure
    Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine.
    limitations
    Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Bos taurus; Rattus norvegicus
    plain_language
    The intervention reduced one pathway fed by excess sugar intermediates.
    primary_references
    [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
    tissue_or_cell_type
    Endothelial cultures and retina

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1891–1901

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High-glucose bovine endothelial cells and diabetic rat retinal experiments. · source_derived_draft · unverified_draft

    ### b1-benfotiamine-hexosamine Benfotiamine inhibited hyperglycemia-associated hexosamine-pathway activation in the tested models. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The intervention reduced one pathway fed by excess sugar intermediates. organism: Bos taurus; Rattus norvegicus tissue_or_cell_type: Endothelial cultures and retina experimental_model: High-glucose bovine endothelial cells and diabetic rat retinal experiments. limitations: Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase. exposure: Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine. [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
    Complete structured claim and evidence

  4. Benfotiamine inhibited hyperglycemia-associated NF-kappaB activation in the tested models.

    Benfotiamine → NF-kappaB family source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    High-glucose bovine endothelial cells and diabetic rat retinal experiments.
    exposure
    Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine.
    limitations
    Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Bos taurus; Rattus norvegicus
    plain_language
    An inflammatory signaling readout also declined in these experiments.
    primary_references
    [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
    tissue_or_cell_type
    Endothelial cultures and retina

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1927–1937

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High-glucose bovine endothelial cells and diabetic rat retinal experiments. · source_derived_draft · unverified_draft

    ### b1-benfotiamine-nfkb Benfotiamine inhibited hyperglycemia-associated NF-kappaB activation in the tested models. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: An inflammatory signaling readout also declined in these experiments. organism: Bos taurus; Rattus norvegicus tissue_or_cell_type: Endothelial cultures and retina experimental_model: High-glucose bovine endothelial cells and diabetic rat retinal experiments. limitations: Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase. exposure: Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine. [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
    Complete structured claim and evidence

  5. Benfotiamine inhibited hyperglycemia-associated DAG-PKC pathway activation in the tested models.

    Benfotiamine → Protein kinase C family source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    High-glucose bovine endothelial cells and diabetic rat retinal experiments.
    exposure
    Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine.
    limitations
    Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Bos taurus; Rattus norvegicus
    plain_language
    Sugar processing was linked to a lipid-signaling pathway response.
    primary_references
    [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
    tissue_or_cell_type
    Endothelial cultures and retina

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1915–1925

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High-glucose bovine endothelial cells and diabetic rat retinal experiments. · source_derived_draft · unverified_draft

    ### b1-benfotiamine-pkc Benfotiamine inhibited hyperglycemia-associated DAG-PKC pathway activation in the tested models. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Sugar processing was linked to a lipid-signaling pathway response. organism: Bos taurus; Rattus norvegicus tissue_or_cell_type: Endothelial cultures and retina experimental_model: High-glucose bovine endothelial cells and diabetic rat retinal experiments. limitations: Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase. exposure: Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine. [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
    Complete structured claim and evidence

  6. Benfotiamine prevented experimental diabetic retinopathy in the rat model reported by Hammes and colleagues.

    Benfotiamine → Diabetic retinal microvascular damage source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    High-glucose bovine endothelial cells and diabetic rat retinal experiments.
    exposure
    Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine.
    limitations
    Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Bos taurus; Rattus norvegicus
    plain_language
    The retinal disease endpoint improved in this animal experiment.
    primary_references
    [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
    tissue_or_cell_type
    Endothelial cultures and retina

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1939–1949

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High-glucose bovine endothelial cells and diabetic rat retinal experiments. · source_derived_draft · unverified_draft

    ### b1-benfotiamine-rat-retinopathy Benfotiamine prevented experimental diabetic retinopathy in the rat model reported by Hammes and colleagues. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The retinal disease endpoint improved in this animal experiment. organism: Bos taurus; Rattus norvegicus tissue_or_cell_type: Endothelial cultures and retina experimental_model: High-glucose bovine endothelial cells and diabetic rat retinal experiments. limitations: Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase. exposure: Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine. [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
    Complete structured claim and evidence

  7. Benfotiamine increased retinal transketolase activity in diabetic rats.

    Benfotiamine → Retinal transketolase activity source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    High-glucose bovine endothelial cells and diabetic rat retinal experiments.
    exposure
    Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine.
    limitations
    Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Bos taurus; Rattus norvegicus
    plain_language
    A B1 derivative increased a carbon-transfer enzyme activity in the diabetic retina.
    primary_references
    [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
    tissue_or_cell_type
    Endothelial cultures and retina

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1879–1889

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High-glucose bovine endothelial cells and diabetic rat retinal experiments. · source_derived_draft · unverified_draft

    ### b1-benfotiamine-tkt Benfotiamine increased retinal transketolase activity in diabetic rats. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A B1 derivative increased a carbon-transfer enzyme activity in the diabetic retina. organism: Bos taurus; Rattus norvegicus tissue_or_cell_type: Endothelial cultures and retina experimental_model: High-glucose bovine endothelial cells and diabetic rat retinal experiments. limitations: Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase. exposure: Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine. [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
    Complete structured claim and evidence

  8. PLCB3 hydrolyzed PI(4,5)P2 to produce soluble IP3 and membrane-associated diacylglycerol.

    PLCB3 (phospholipase C beta 3) → IP3 source_derived_draftungraded
    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
    Splitting one membrane lipid creates two different signaling products.
    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 626–637

    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-plc-ip3 PLCB3 hydrolyzed PI(4,5)P2 to produce soluble IP3 and membrane-associated diacylglycerol. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: Splitting one membrane lipid creates two different signaling products. 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

  9. SELENOI transfers phosphoethanolamine from CDP-ethanolamine to diacylglycerol, producing diacyl PE and CMP.

    SELENOI → Phosphatidylethanolamine source_derived_draftliterature_reviewed:direct_experimental
    Experimental context and source evidence
    cell_type
    patient fibroblasts and HeLa
    experimental_model
    Lipid synthesis and genetic studies
    limitations
    Other enzymes can contribute to diacyl PE.
    organism
    human

    Selenium: literature corrections and mechanism additions · lines 726–736

    Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Lipid synthesis and genetic studies · secondary_verified · secondary_verified

    ## selenoi-synthesizes-diacyl-pe SELENOI builds phosphatidylethanolamine from an activated headgroup and a lipid backbone. SELENOI transfers phosphoethanolamine from CDP-ethanolamine to diacylglycerol, producing diacyl PE and CMP. Organism: human Cell type: patient fibroblasts and HeLa Experimental model: Lipid synthesis and genetic studies Limitations: Other enzymes can contribute to diacyl PE. Primary reference: [EPT1 (selenoprotein I) is critical for the neural development and maintenance of plasmalogen in humans](https://pmc.ncbi.nlm.nih.gov/articles/PMC5983406/)
    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.

    Evidence, AI assistance and curation standards