Component

Phosphatidylethanolamine

The membrane lipid proposed as a convergence point.

12 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. CEPT1 also catalyzes phosphatidylethanolamine production, unlike the human CHPT1 specificity described in the study.

    Human choline/ethanolamine phosphotransferase 1 / CEPT1 → Phosphatidylethanolamine 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
    The related enzymes are not interchangeable in substrate preference.
    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 789–800

    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-cept1-pe CEPT1 also catalyzes phosphatidylethanolamine production, unlike the human CHPT1 specificity described in the study. Condition category: normal nutrient_topic: Choline research collection; topical membership is not evidence of a direct dietary effect. plain_language: The related enzymes are not interchangeable in substrate preference. 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. PEMT converts PE to PC through three sequential SAM-dependent methylation reactions.

    Human phosphatidylethanolamine N-methyltransferase / PEMT → Phosphatidylethanolamine source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/choline-research/12431977.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c299a547408772f2f24bdd77f2f22dc8ea9e5aaf8179150f2d8b59c9713306a", "start_char": 0, "end_char": 1380, "text_sha256": "7c299a547408772f2f24bdd77f2f22dc8ea9e5aaf8179150f2d8b59c9713306a"}
    experimental_model
    Human liver fractionation and recombinant PEMT membrane-topology experiments
    exposure
    Protein cleavage mapping and methyltransferase localization
    limitations
    Three methyl transfers make a choline-containing phospholipid; PEMT does not directly synthesize free choline from nothing.
    nutrient_topic
    Choline research collection; topical membership is not evidence of a direct dietary effect. · Choline
    organism
    Human enzyme
    plain_language
    The body can build a choline headgroup in a membrane lipid by spending methyl groups.
    primary_references
    [choline-p12431977] Membrane topography of human phosphatidylethanolamine N-methyltransferase. (2003). https://pubmed.ncbi.nlm.nih.gov/12431977/ DOI: 10.1074/jbc.m210904200
    tissue_or_cell_type
    ER and mitochondria-associated membranes

    Choline: metabolism, signaling and nutrient connections (2026-09-17) · lines 802–813

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human liver fractionation and recombinant PEMT membrane-topology experiments · source_derived_draft · unverified_draft

    ### choline-pemt-pc PEMT converts PE to PC through three sequential SAM-dependent methylation reactions. Condition category: normal nutrient_topic: Choline research collection; topical membership is not evidence of a direct dietary effect. plain_language: The body can build a choline headgroup in a membrane lipid by spending methyl groups. organism: Human enzyme tissue_or_cell_type: ER and mitochondria-associated membranes experimental_model: Human liver fractionation and recombinant PEMT membrane-topology experiments limitations: Three methyl transfers make a choline-containing phospholipid; PEMT does not directly synthesize free choline from nothing. exposure: Protein cleavage mapping and methyltransferase localization evidence_span: {"source_cache": "artifacts/choline-research/12431977.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c299a547408772f2f24bdd77f2f22dc8ea9e5aaf8179150f2d8b59c9713306a", "start_char": 0, "end_char": 1380, "text_sha256": "7c299a547408772f2f24bdd77f2f22dc8ea9e5aaf8179150f2d8b59c9713306a"} [choline-p12431977] Membrane topography of human phosphatidylethanolamine N-methyltransferase. (2003). https://pubmed.ncbi.nlm.nih.gov/12431977/ DOI: 10.1074/jbc.m210904200
    Complete structured claim and evidence

  3. Human PISD converts phosphatidylserine to phosphatidylethanolamine in the inner mitochondrial membrane; patient fibroblasts with PISD variants showed reduced conversion.

    Human phosphatidylserine decarboxylase / PISD → Phosphatidylethanolamine source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human family genetics and fibroblast lipid-conversion measurements.
    limitations
    This pathway uses membrane-bound phosphatidylserine, not free serine as the direct PISD substrate.
    nutrient_topic
    L-Serine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Serine
    plain_language
    A serine-derived lipid feeds another lipid needed inside mitochondria.
    primary_references
    PISD is a mitochondrial disease gene causing skeletal dysplasia, cataracts, and white matter changes. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30858161/ · DOI 10.26508/lsa.201900353

    L-Serine: synthesis, one-carbon metabolism, lipids and cross-nutrient mechanisms (2026-09-19) · lines 422–428

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human family genetics and fibroblast lipid-conversion measurements. · source_derived_draft · unverified_draft

    ## l-serine-pisd-decarboxylation A serine-derived lipid feeds another lipid needed inside mitochondria. Human PISD converts phosphatidylserine to phosphatidylethanolamine in the inner mitochondrial membrane; patient fibroblasts with PISD variants showed reduced conversion. Model: Human family genetics and fibroblast lipid-conversion measurements. Limitations: This pathway uses membrane-bound phosphatidylserine, not free serine as the direct PISD substrate. Evidence access: Primary abstract PISD is a mitochondrial disease gene causing skeletal dysplasia, cataracts, and white matter changes. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30858161/ · DOI 10.26508/lsa.201900353
    Complete structured claim and evidence

  4. Reconstituted ABCA4 also transported phosphatidylethanolamine in the import orientation.

    ABCA4 retinoid transporter → Phosphatidylethanolamine source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Fluorescent lipid transport
    limitations
    Lipid transport alone does not prove the complete visual-cycle flux.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Purified/reconstituted transporter
    plain_language
    The transporter can move PE as well as its retinal adduct.
    primary_references
    [quazi-2012] ABCA4 is an N-retinylidene-phosphatidylethanolamine and phosphatidylethanolamine importer (2012). https://pmc.ncbi.nlm.nih.gov/articles/PMC3871175/ DOI: 10.1038/ncomms1927
    tissue_or_cell_type
    Model membranes
    transport_direction
    lumen-equivalent leaflet to cytoplasmic-equivalent leaflet
    transport_effect
    raises Recorded as transport in the import orientation in the reconstituted system.
    transport_pool
    the cytoplasmic leaflet of the disc membrane Recorded as transport in the import orientation in the reconstituted system.

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 813–823

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Fluorescent lipid transport · source_derived_draft · unverified_draft

    ### a-vision-abca4-pe-flip Reconstituted ABCA4 also transported phosphatidylethanolamine in the import orientation. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: The transporter can move PE as well as its retinal adduct. organism: Purified/reconstituted transporter tissue_or_cell_type: Model membranes experimental_model: Fluorescent lipid transport limitations: Lipid transport alone does not prove the complete visual-cycle flux. transport_direction: lumen-equivalent leaflet to cytoplasmic-equivalent leaflet [quazi-2012] ABCA4 is an N-retinylidene-phosphatidylethanolamine and phosphatidylethanolamine importer (2012). https://pmc.ncbi.nlm.nih.gov/articles/PMC3871175/ DOI: 10.1038/ncomms1927
    Complete structured claim and evidence

  5. SELENOI, GPX4, and SELENOK may converge on phosphatidylethanolamine synthesis, protection, and calcium-linked peroxidation control.

    SELENOK → Phosphatidylethanolamine hypothesisunverified_cross_path_inference
    Experimental context and source evidence

    Selenium corrections and deep dive · lines 446–448

    Selenium correction and deep-dive draft · supports · Source draft; model details require primary-source verification · source_derived_draft · unverified_draft

    **4. The PE circuit.** SELENOI **makes** PE. GPX4 **protects** PE. SELENOK **enables palmitoylation of IP3R**, which controls the Ca²⁺ flux that drives lipid peroxidation. Three selenoproteins, three different verbs, one lipid. SELENOI mutations cause **SPG81 spastic paraplegia**; GPX4 loss causes **interneuron death**. Both neurological, both PE. Nobody has assayed them as one circuit. **If I were hunting for something undiscovered, this is where I'd put the money.**
    Complete structured claim and evidence

  6. 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

Where it participates (unsigned role)

  1. Experimental manipulation supported a causal role for the lowered PC/PE ratio in loss of hepatocyte membrane integrity.

    Mouse hepatic phosphatidylcholine/phosphatidylethanolamine ratio → Mouse hepatocyte membrane integrity source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/choline-research/16679290.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "656910ebe959c2867cac5d7cb75341ba3974ff922e584274829161326f10cf4d", "start_char": 0, "end_char": 1016, "text_sha256": "656910ebe959c2867cac5d7cb75341ba3974ff922e584274829161326f10cf4d"}
    experimental_model
    Dietary depletion and Pemt/Mdr2 mouse genetics
    exposure
    Choline-deficient feeding in Pemt-null and double-null mice
    limitations
    A combined diet/genotype model; total PC amount, PC/PE ratio and membrane damage are not interchangeable measurements.
    nutrient_topic
    Choline research collection; topical membership is not evidence of a direct dietary effect. · Choline
    organism
    Mouse, with separate human tissue comparison in the paper
    plain_language
    The balance between two membrane lipids mattered, not just one concentration.
    primary_references
    [choline-p16679290] The ratio of phosphatidylcholine to phosphatidylethanolamine influences membrane integrity and steatohepatitis. (2006). https://pubmed.ncbi.nlm.nih.gov/16679290/ DOI: 10.1016/j.cmet.2006.03.007
    tissue_or_cell_type
    Hepatic membranes
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Choline: metabolism, signaling and nutrient connections (2026-09-17) · lines 906–917

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dietary depletion and Pemt/Mdr2 mouse genetics · source_derived_draft · unverified_draft

    ### choline-pc-pe-membrane Experimental manipulation supported a causal role for the lowered PC/PE ratio in loss of hepatocyte membrane integrity. Condition category: nutrient_deficiency nutrient_topic: Choline research collection; topical membership is not evidence of a direct dietary effect. plain_language: The balance between two membrane lipids mattered, not just one concentration. organism: Mouse, with separate human tissue comparison in the paper tissue_or_cell_type: Hepatic membranes experimental_model: Dietary depletion and Pemt/Mdr2 mouse genetics limitations: A combined diet/genotype model; total PC amount, PC/PE ratio and membrane damage are not interchangeable measurements. exposure: Choline-deficient feeding in Pemt-null and double-null mice evidence_span: {"source_cache": "artifacts/choline-research/16679290.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "656910ebe959c2867cac5d7cb75341ba3974ff922e584274829161326f10cf4d", "start_char": 0, "end_char": 1016, "text_sha256": "656910ebe959c2867cac5d7cb75341ba3974ff922e584274829161326f10cf4d"} [choline-p16679290] The ratio of phosphatidylcholine to phosphatidylethanolamine influences membrane integrity and steatohepatitis. (2006). https://pubmed.ncbi.nlm.nih.gov/16679290/ DOI: 10.1016/j.cmet.2006.03.007
    Complete structured claim and evidence

  2. SAM supplies the methyl groups for each of the three PEMT-catalyzed transfers.

    S-Adenosyl-L-methionine → Human phosphatidylethanolamine N-methyltransferase / PEMT source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/choline-research/12431977.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c299a547408772f2f24bdd77f2f22dc8ea9e5aaf8179150f2d8b59c9713306a", "start_char": 0, "end_char": 1380, "text_sha256": "7c299a547408772f2f24bdd77f2f22dc8ea9e5aaf8179150f2d8b59c9713306a"}
    experimental_model
    Human liver fractionation and recombinant PEMT membrane-topology experiments
    exposure
    Protein cleavage mapping and methyltransferase localization
    limitations
    Three methyl transfers make a choline-containing phospholipid; PEMT does not directly synthesize free choline from nothing.
    nutrient_topic
    Choline research collection; topical membership is not evidence of a direct dietary effect. · Choline
    organism
    Human enzyme
    plain_language
    Membrane PC synthesis and the methyl-donor pool are connected.
    primary_references
    [choline-p12431977] Membrane topography of human phosphatidylethanolamine N-methyltransferase. (2003). https://pubmed.ncbi.nlm.nih.gov/12431977/ DOI: 10.1074/jbc.m210904200
    tissue_or_cell_type
    ER and mitochondria-associated membranes

    Choline: metabolism, signaling and nutrient connections (2026-09-17) · lines 815–826

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human liver fractionation and recombinant PEMT membrane-topology experiments · source_derived_draft · unverified_draft

    ### choline-pemt-sam SAM supplies the methyl groups for each of the three PEMT-catalyzed transfers. Condition category: normal nutrient_topic: Choline research collection; topical membership is not evidence of a direct dietary effect. plain_language: Membrane PC synthesis and the methyl-donor pool are connected. organism: Human enzyme tissue_or_cell_type: ER and mitochondria-associated membranes experimental_model: Human liver fractionation and recombinant PEMT membrane-topology experiments limitations: Three methyl transfers make a choline-containing phospholipid; PEMT does not directly synthesize free choline from nothing. exposure: Protein cleavage mapping and methyltransferase localization evidence_span: {"source_cache": "artifacts/choline-research/12431977.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c299a547408772f2f24bdd77f2f22dc8ea9e5aaf8179150f2d8b59c9713306a", "start_char": 0, "end_char": 1380, "text_sha256": "7c299a547408772f2f24bdd77f2f22dc8ea9e5aaf8179150f2d8b59c9713306a"} [choline-p12431977] Membrane topography of human phosphatidylethanolamine N-methyltransferase. (2003). https://pubmed.ncbi.nlm.nih.gov/12431977/ DOI: 10.1074/jbc.m210904200
    Complete structured claim and evidence

  3. PISD patient fibroblasts had fragmented mitochondria, enlarged lysosomes and reduced maximal oxygen consumption; one variant impaired the enzyme autocatalytic processing required for activity.

    Human phosphatidylserine decarboxylase / PISD → Mitochondrial function in PISD patient fibroblasts source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Two affected sisters, patient fibroblasts and functional variant characterization.
    limitations
    The other allele produced an alternative splice product; different molecular defects remain distinct.
    nutrient_topic
    L-Serine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Serine
    plain_language
    A downstream processing defect can persist despite precursor availability.
    primary_references
    PISD is a mitochondrial disease gene causing skeletal dysplasia, cataracts, and white matter changes. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30858161/ · DOI 10.26508/lsa.201900353
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Serine: synthesis, one-carbon metabolism, lipids and cross-nutrient mechanisms (2026-09-19) · lines 430–436

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Two affected sisters, patient fibroblasts and functional variant characterization. · source_derived_draft · unverified_draft

    ## l-serine-pisd-failure A downstream processing defect can persist despite precursor availability. PISD patient fibroblasts had fragmented mitochondria, enlarged lysosomes and reduced maximal oxygen consumption; one variant impaired the enzyme autocatalytic processing required for activity. Model: Two affected sisters, patient fibroblasts and functional variant characterization. Limitations: The other allele produced an alternative splice product; different molecular defects remain distinct. Evidence access: Primary abstract PISD is a mitochondrial disease gene causing skeletal dysplasia, cataracts, and white matter changes. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30858161/ · DOI 10.26508/lsa.201900353
    Complete structured claim and evidence

  4. Lyso-PE treatment and genetic complementation restored mitochondrial and lysosomal morphology in PISD patient fibroblasts.

    Lysophosphatidylethanolamine → Organelle morphology in PISD patient fibroblasts source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Human patient fibroblast rescue experiments.
    limitations
    This is not evidence that oral serine or phosphatidylserine corrects PISD disease.
    nutrient_topic
    L-Serine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Serine
    plain_language
    Supplying a downstream lipid can bypass a specific defect in culture.
    primary_references
    PISD is a mitochondrial disease gene causing skeletal dysplasia, cataracts, and white matter changes. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30858161/ · DOI 10.26508/lsa.201900353
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Serine: synthesis, one-carbon metabolism, lipids and cross-nutrient mechanisms (2026-09-19) · lines 438–444

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human patient fibroblast rescue experiments. · source_derived_draft · unverified_draft

    ## l-serine-pisd-lipid-rescue Supplying a downstream lipid can bypass a specific defect in culture. Lyso-PE treatment and genetic complementation restored mitochondrial and lysosomal morphology in PISD patient fibroblasts. Model: Human patient fibroblast rescue experiments. Limitations: This is not evidence that oral serine or phosphatidylserine corrects PISD disease. Evidence access: Primary abstract PISD is a mitochondrial disease gene causing skeletal dysplasia, cataracts, and white matter changes. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30858161/ · DOI 10.26508/lsa.201900353
    Complete structured claim and evidence

  5. Purified human PSS2 converted phosphatidylethanolamine, but not phosphatidylcholine, into phosphatidylserine; added phosphatidylserine inhibited purified PSS2.

    Human phosphatidylserine synthase 2 / PTDSS2 → Phosphatidylserine source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Purified epitope-tagged human PSS1/PSS2 substrate and feedback assays.
    limitations
    In this preparation PSS1 used both PC and PE and was not inhibited by added PS; purified-enzyme feedback cannot be assumed identical across preparations or intact cells.
    nutrient_topic
    L-Serine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Serine
    plain_language
    A second enzyme uses a different membrane-lipid starting material.
    primary_references
    Purification and characterization of human phosphatidylserine synthases 1 and 2. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19014349/ · DOI 10.1042/BJ20081597

    L-Serine: synthesis, one-carbon metabolism, lipids and cross-nutrient mechanisms (2026-09-19) · lines 414–420

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Purified epitope-tagged human PSS1/PSS2 substrate and feedback assays. · source_derived_draft · unverified_draft

    ## l-serine-pss2-exchange A second enzyme uses a different membrane-lipid starting material. Purified human PSS2 converted phosphatidylethanolamine, but not phosphatidylcholine, into phosphatidylserine; added phosphatidylserine inhibited purified PSS2. Model: Purified epitope-tagged human PSS1/PSS2 substrate and feedback assays. Limitations: In this preparation PSS1 used both PC and PE and was not inhibited by added PS; purified-enzyme feedback cannot be assumed identical across preparations or intact cells. Evidence access: Primary abstract Purification and characterization of human phosphatidylserine synthases 1 and 2. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19014349/ · DOI 10.1042/BJ20081597
    Complete structured claim and evidence

  6. ABCA4 drove ATP-dependent transport of retinal-PE adduct from the disc lumen-facing leaflet toward the cytoplasmic leaflet.

    ABCA4 retinoid transporter → N-retinylidene-phosphatidylethanolamine source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Proteoliposomes and native disc transport assays
    limitations
    The assayed substrate is the adduct, not a requirement for free retinal diffusion.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Bovine/mouse discs; recombinant transporter
    plain_language
    ABCA4 moves the trapped retinal-lipid adduct to the disposal side of the disc.
    primary_references
    [quazi-2012] ABCA4 is an N-retinylidene-phosphatidylethanolamine and phosphatidylethanolamine importer (2012). https://pmc.ncbi.nlm.nih.gov/articles/PMC3871175/ DOI: 10.1038/ncomms1927
    tissue_or_cell_type
    Photoreceptor disc membrane
    transport_direction
    disc lumen leaflet to cytoplasmic leaflet
    transport_effect
    raises Recorded as ATP-dependent transport from the disc lumen-facing leaflet toward the cytoplasmic leaflet.
    transport_pool
    the cytoplasmic leaflet of the disc membrane Recorded as ATP-dependent transport from the disc lumen-facing leaflet toward the cytoplasmic leaflet.

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 801–811

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Proteoliposomes and native disc transport assays · source_derived_draft · unverified_draft

    ### a-vision-abca4-retinoid-flip ABCA4 drove ATP-dependent transport of retinal-PE adduct from the disc lumen-facing leaflet toward the cytoplasmic leaflet. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: ABCA4 moves the trapped retinal-lipid adduct to the disposal side of the disc. organism: Bovine/mouse discs; recombinant transporter tissue_or_cell_type: Photoreceptor disc membrane experimental_model: Proteoliposomes and native disc transport assays limitations: The assayed substrate is the adduct, not a requirement for free retinal diffusion. transport_direction: disc lumen leaflet to cytoplasmic leaflet [quazi-2012] ABCA4 is an N-retinylidene-phosphatidylethanolamine and phosphatidylethanolamine importer (2012). https://pmc.ncbi.nlm.nih.gov/articles/PMC3871175/ DOI: 10.1038/ncomms1927
    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