Component

Mouse Slc23a2 gene

Mouse gene encoding SVCT2; distinct from its protein. The SVCT2 gene was historically called Slc23a1 in Sotiriou 2002.

3 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.

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 it acts on

  1. Embryonic fibroblasts from SVCT2-null mice retained less than 5% of normal ascorbic-acid uptake.

    Mouse Slc23a2 gene → Cellular ascorbate uptake source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    SVCT2-null mouse embryos, newborns and embryonic fibroblasts
    exposure
    Homozygous SVCT2 gene deletion
    limitations
    Historical gene naming corrected to Slc23a2; abstract-limited assay details.
    nutrient_topic
    Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
    organism
    Mus musculus
    plain_language
    Without SVCT2, these embryonic cells took up very little reduced vitamin C.
    primary_references
    [sotiriou2002] Ascorbic-acid transporter Slc23a1 is essential for vitamin C transport into the brain and for perinatal survival. (2002). https://pubmed.ncbi.nlm.nih.gov/11984597/ DOI: 10.1038/0502-514
    tissue_or_cell_type
    Embryonic fibroblasts
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 208–219

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SVCT2-null mouse embryos, newborns and embryonic fibroblasts · source_derived_draft · unverified_draft

    ### vc-transport-svct2-fibroblast-loss Embryonic fibroblasts from SVCT2-null mice retained less than 5% of normal ascorbic-acid uptake. Condition category: machinery_impairment nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: Without SVCT2, these embryonic cells took up very little reduced vitamin C. organism: Mus musculus tissue_or_cell_type: Embryonic fibroblasts experimental_model: SVCT2-null mouse embryos, newborns and embryonic fibroblasts limitations: Historical gene naming corrected to Slc23a2; abstract-limited assay details. exposure: Homozygous SVCT2 gene deletion cross_nutrient: false [sotiriou2002] Ascorbic-acid transporter Slc23a1 is essential for vitamin C transport into the brain and for perinatal survival. (2002). https://pubmed.ncbi.nlm.nih.gov/11984597/ DOI: 10.1038/0502-514
    Complete structured claim and evidence
  2. SVCT2-null mice died within minutes of birth with respiratory failure and intraparenchymal brain hemorrhage.

    Mouse Slc23a2 gene → Perinatal survival source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    SVCT2-null mouse embryos, newborns and embryonic fibroblasts
    exposure
    Homozygous SVCT2 gene deletion
    limitations
    Multiorgan model; hemorrhage was not simply established as generalized scurvy, and individual lethal pathways were not isolated.
    nutrient_topic
    Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
    organism
    Mus musculus
    plain_language
    Severe loss of cellular vitamin C transport was lethal around birth in mice.
    primary_references
    [sotiriou2002] Ascorbic-acid transporter Slc23a1 is essential for vitamin C transport into the brain and for perinatal survival. (2002). https://pubmed.ncbi.nlm.nih.gov/11984597/ DOI: 10.1038/0502-514
    tissue_or_cell_type
    Newborn brain and lung
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 221–232

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SVCT2-null mouse embryos, newborns and embryonic fibroblasts · source_derived_draft · unverified_draft

    ### vc-transport-svct2-neonatal-phenotype SVCT2-null mice died within minutes of birth with respiratory failure and intraparenchymal brain hemorrhage. Condition category: machinery_impairment nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: Severe loss of cellular vitamin C transport was lethal around birth in mice. organism: Mus musculus tissue_or_cell_type: Newborn brain and lung experimental_model: SVCT2-null mouse embryos, newborns and embryonic fibroblasts limitations: Multiorgan model; hemorrhage was not simply established as generalized scurvy, and individual lethal pathways were not isolated. exposure: Homozygous SVCT2 gene deletion cross_nutrient: false [sotiriou2002] Ascorbic-acid transporter Slc23a1 is essential for vitamin C transport into the brain and for perinatal survival. (2002). https://pubmed.ncbi.nlm.nih.gov/11984597/ DOI: 10.1038/0502-514
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Maternal prenatal ascorbic-acid supplementation did not raise fetal blood ascorbate in SVCT2-null mouse fetuses.

    L-Ascorbate → Fetal blood ascorbate concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    SVCT2-null mouse embryos, newborns and embryonic fibroblasts
    exposure
    Prenatal maternal supplementation with SVCT2-null fetuses
    limitations
    Supports a placental transport role but is not a placenta-specific deletion; dose is not resolved in the accessible abstract.
    nutrient_topic
    Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
    organism
    Mus musculus
    plain_language
    Increasing maternal supply did not overcome the fetus’s missing SVCT2 machinery.
    primary_references
    [sotiriou2002] Ascorbic-acid transporter Slc23a1 is essential for vitamin C transport into the brain and for perinatal survival. (2002). https://pubmed.ncbi.nlm.nih.gov/11984597/ DOI: 10.1038/0502-514
    tissue_or_cell_type
    Placenta/fetal blood
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 234–245

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SVCT2-null mouse embryos, newborns and embryonic fibroblasts · source_derived_draft · unverified_draft

    ### vc-transport-svct2-prenatal-nonrescue Maternal prenatal ascorbic-acid supplementation did not raise fetal blood ascorbate in SVCT2-null mouse fetuses. Condition category: machinery_impairment nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: Increasing maternal supply did not overcome the fetus’s missing SVCT2 machinery. organism: Mus musculus tissue_or_cell_type: Placenta/fetal blood experimental_model: SVCT2-null mouse embryos, newborns and embryonic fibroblasts limitations: Supports a placental transport role but is not a placenta-specific deletion; dose is not resolved in the accessible abstract. exposure: Prenatal maternal supplementation with SVCT2-null fetuses cross_nutrient: false [sotiriou2002] Ascorbic-acid transporter Slc23a1 is essential for vitamin C transport into the brain and for perinatal survival. (2002). https://pubmed.ncbi.nlm.nih.gov/11984597/ DOI: 10.1038/0502-514
    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