Component

Mouse Slc25a32 mitochondrial carrier

Mouse mitochondrial carrier studied in flavin and folate uptake assays. Mouse Slc25a32 carrier studied by transport and metabolic assays.

4 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 it acts on

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

    Mouse Slc25a32 mitochondrial carrier → Mitochondrial folate uptake source_derived_draftungraded
    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

Where it participates (unsigned role)

  1. DLD activity in Slc25a32-null embryo mitochondria was about 23.9% of wild-type control.

    Slc25a32-null mouse genotype → Mouse dihydrolipoamide dehydrogenase / Dld source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    DLD links B2 cofactor supply to glycine cleavage and thus folate-mediated one-carbon metabolism.
    evidence_spans
    [{"source_bundle": "artifacts/riboflavin_metabolism_sources.json", "source_key": "PMC11072207", "locator": "HTML article p", "paragraph_index": 43, "char_start": 0, "char_end": 1215, "evidence_access": "full-text"}]
    experimental_model
    Slc25a32-null embryos and missense knock-in mice, isolated mitochondria and skeletal-muscle enzyme assays.
    exposure
    Slc25a32-null versus wild-type embryos.
    limitations
    Knockout affects multiple flavoproteins; DLD-specific genetic rescue was not performed.
    nutrient_topic
    Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
    organism
    Mus musculus
    plain_language
    A defect in mitochondrial flavin supply impaired the shared DLD enzyme.
    primary_references
    [peng-2022-slc25a32] Mitochondrial FAD shortage in SLC25A32 deficiency affects folate-mediated one-carbon metabolism (2022). https://pubmed.ncbi.nlm.nih.gov/35727412/ DOI: 10.1007/s00018-022-04404-0
    tissue_or_cell_type
    Embryo mitochondria
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 874–886

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Slc25a32-null embryos and missense knock-in mice, isolated mitochondria and skeletal-muscle enzyme assays. · source_derived_draft · unverified_draft

    ### b2-met-mouse-null-dld-activity DLD activity in Slc25a32-null embryo mitochondria was about 23.9% of wild-type control. Condition category: machinery_impairment nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A defect in mitochondrial flavin supply impaired the shared DLD enzyme. organism: Mus musculus tissue_or_cell_type: Embryo mitochondria experimental_model: Slc25a32-null embryos and missense knock-in mice, isolated mitochondria and skeletal-muscle enzyme assays. limitations: Knockout affects multiple flavoproteins; DLD-specific genetic rescue was not performed. exposure: Slc25a32-null versus wild-type embryos. cross_nutrient: DLD links B2 cofactor supply to glycine cleavage and thus folate-mediated one-carbon metabolism. evidence_spans: [{"source_bundle": "artifacts/riboflavin_metabolism_sources.json", "source_key": "PMC11072207", "locator": "HTML article p", "paragraph_index": 43, "char_start": 0, "char_end": 1215, "evidence_access": "full-text"}] [peng-2022-slc25a32] Mitochondrial FAD shortage in SLC25A32 deficiency affects folate-mediated one-carbon metabolism (2022). https://pubmed.ncbi.nlm.nih.gov/35727412/ DOI: 10.1007/s00018-022-04404-0
    Complete structured claim and evidence

  2. K235R/K235R and Y174C/K235R mouse muscle mitochondria accumulated less isotope-labeled FAD; Slc25a32-null embryonic mitochondria also had impaired FAD uptake.

    Slc25a32 K235R-containing mouse genotypes → Mitochondrial FAD uptake source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_location
    Figure 5C-D
    experimental_model
    Stable-isotope uptake in isolated knock-in/knockout mitochondria
    exposure
    10 micromolar isotope-labeled FAD; knockout embryo endpoint at 60 minutes.
    limitations
    Organelle uptake supports carrier dependence but does not establish exchange partner or transport stoichiometry.
    nutrient_topic
    Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
    organism
    Mus musculus
    plain_language
    The carrier defect restricts access to mitochondrial FAD.
    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
    Skeletal muscle and embryonic mitochondria
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 490–501

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Stable-isotope uptake in isolated knock-in/knockout mitochondria · source_derived_draft · unverified_draft

    ### transport-slc25a32-fad-import K235R/K235R and Y174C/K235R mouse muscle mitochondria accumulated less isotope-labeled FAD; Slc25a32-null embryonic mitochondria also had impaired FAD uptake. Condition category: machinery_impairment nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The carrier defect restricts access to mitochondrial FAD. organism: Mus musculus tissue_or_cell_type: Skeletal muscle and embryonic mitochondria experimental_model: Stable-isotope uptake in isolated knock-in/knockout mitochondria limitations: Organelle uptake supports carrier dependence but does not establish exchange partner or transport stoichiometry. exposure: 10 micromolar isotope-labeled FAD; knockout embryo endpoint at 60 minutes. evidence_location: Figure 5C-D [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

  3. The tested Slc25a32 mutant muscle mitochondria did not show impaired uptake of isotope-labeled free riboflavin.

    Slc25a32 K235R-containing mouse genotypes → Mitochondrial riboflavin uptake source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_location
    Figure 5C
    experimental_model
    Stable-isotope riboflavin uptake in isolated muscle mitochondria
    exposure
    10 micromolar labeled riboflavin.
    limitations
    The identity of the preserved riboflavin-entry route was not established.
    nutrient_topic
    Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
    organism
    Mus musculus
    plain_language
    A mitochondrial FAD transport defect need not be a free-riboflavin import defect.
    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
    Skeletal-muscle mitochondria
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 503–514

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

    ### transport-slc25a32-riboflavin-selectivity The tested Slc25a32 mutant muscle mitochondria did not show impaired uptake of isotope-labeled free riboflavin. Condition category: machinery_impairment nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A mitochondrial FAD transport defect need not be a free-riboflavin import defect. organism: Mus musculus tissue_or_cell_type: Skeletal-muscle mitochondria experimental_model: Stable-isotope riboflavin uptake in isolated muscle mitochondria limitations: The identity of the preserved riboflavin-entry route was not established. exposure: 10 micromolar labeled riboflavin. evidence_location: Figure 5C [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.

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