Component
Cellular ascorbate uptake
Cellular ascorbate uptake
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 acts on it
In patient-derived primary acute-myeloid-leukaemia cells, vitamin C restored TET2 activity only when SLC2A3 was expressed, and SLC2A3 knockdown in the KG-1 cell line decreased the response to vitamin C.
Experimental context and source evidence
- duration
- Culture experiments
- experimental_model
- AML cell lines, an SLC2A3-knockdown line and patient-derived primary AML cells; TCGA and TARGET expression analysis
- exposure
- Vitamin C, with and without SLC2A3 knockdown
- limitations
- Below-median SLC2A3 expression was associated with poorer overall survival, which is an association within a database cohort and not an experimental outcome.
- organism
- Homo sapiens
- plain_language
- If the cell cannot take vitamin C in, the vitamin cannot restore the enzyme.
- primary_references
- [liu-2020] Decreased vitamin C uptake mediated by SLC2A3 promotes leukaemia progression and impedes TET2 restoration (2020). https://pubmed.ncbi.nlm.nih.gov/32203209/ DOI: 10.1038/s41416-020-0788-8
- tissue
- Leukaemic blasts
TET2 loss and malignancy: the step between a nutrient-responsive enzyme and the disease (2026-09-23) · lines 163–171
Original AI-assisted curation of twelve primary studies located by Europe PMC title search, with every statement drafted from the retrieved abstract. Two pairs share a laboratory and are recorded as one line of evidence each. Genetic loss of function, pharmacological exposure and dietary depletion are kept as separate record types. Not publisher full text. · supports · AML cell lines, an SLC2A3-knockdown line and patient-derived primary AML cells; TCGA and TARGET expression analysis · source_derived_draft · unverified_draft
## slc2a3-gates-vitamin-c-tet2-restoration In patient-derived primary acute-myeloid-leukaemia cells, vitamin C restored TET2 activity only when SLC2A3 was expressed, and SLC2A3 knockdown in the KG-1 cell line decreased the response to vitamin C. Model/species: AML cell lines, an SLC2A3-knockdown line and patient-derived primary AML cells; TCGA and TARGET expression analysis Organism: Homo sapiens Tissue/system: Leukaemic blasts Exposure: Vitamin C, with and without SLC2A3 knockdown Duration: Culture experiments Limits: Below-median SLC2A3 expression was associated with poorer overall survival, which is an association within a database cohort and not an experimental outcome. Primary reference: [liu-2020] Decreased vitamin C uptake mediated by SLC2A3 promotes leukaemia progression and impedes TET2 restoration (2020). https://pubmed.ncbi.nlm.nih.gov/32203209/ DOI: 10.1038/s41416-020-0788-8
Complete structured claim and evidenceEmbryonic fibroblasts from SVCT2-null mice retained less than 5% of normal ascorbic-acid uptake.
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
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.