Component

Mitochondrial folate uptake

Uptake of folate substrates by isolated mitochondria.

1 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 acts on it

  1. Slc25a32 mutant and knockout mitochondrial preparations retained folate-substrate uptake in the 2022 mouse study.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Separates primary flavin import from secondary folate-pool changes.
    evidence_location
    Abstract and folate-uptake experiments
    experimental_model
    Folate uptake in genetically altered isolated mitochondria
    exposure
    Labeled folic acid or 5-formyltetrahydrofolate in mitochondrial uptake assays.
    limitations
    Preserved uptake in this model does not fully resolve older human-cDNA complementation results.
    nutrient_topic
    Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
    organism
    Mus musculus
    plain_language
    The mouse experiments attributed the primary import defect to FAD, with folate uptake preserved.
    primary_references
    [transport-slc25a32-2022] Mitochondrial FAD shortage in SLC25A32 deficiency affects folate-mediated one-carbon metabolism. (2022). https://pmc.ncbi.nlm.nih.gov/articles/PMC11072207/ DOI: 10.1007/s00018-022-04404-0
    tissue_or_cell_type
    Muscle and embryonic mitochondria
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 516–528

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Folate uptake in genetically altered isolated mitochondria · source_derived_draft · unverified_draft

    ### transport-slc25a32-folate-uptake-preserved Slc25a32 mutant and knockout mitochondrial preparations retained folate-substrate uptake in the 2022 mouse study. Condition category: machinery_impairment nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The mouse experiments attributed the primary import defect to FAD, with folate uptake preserved. organism: Mus musculus tissue_or_cell_type: Muscle and embryonic mitochondria experimental_model: Folate uptake in genetically altered isolated mitochondria limitations: Preserved uptake in this model does not fully resolve older human-cDNA complementation results. exposure: Labeled folic acid or 5-formyltetrahydrofolate in mitochondrial uptake assays. cross_nutrient: Separates primary flavin import from secondary folate-pool changes. evidence_location: Abstract and folate-uptake experiments [transport-slc25a32-2022] Mitochondrial FAD shortage in SLC25A32 deficiency affects folate-mediated one-carbon metabolism. (2022). https://pmc.ncbi.nlm.nih.gov/articles/PMC11072207/ DOI: 10.1007/s00018-022-04404-0
    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