Component

Mouse Slc25a32 Lys235Arg homozygous genotype

Homozygous K235R knock-in used by Peng 2022.

3 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

Where it participates (unsigned role)

  1. FAD added to muscle assays only mildly improved depressed MCAD activity in Slc25a32 mutant mice; MCAD protein abundance was also lower in K235R homozygotes.

    FAD → Mouse medium-chain acyl-CoA dehydrogenase / Acadm source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_spans
    [{"source_bundle": "artifacts/riboflavin_metabolism_sources.json", "source_key": "PMC11072207", "locator": "HTML article p", "paragraph_index": 50, "char_start": 0, "char_end": 1147, "evidence_access": "full-text"}]
    experimental_model
    Slc25a32-null embryos and missense knock-in mice, isolated mitochondria and skeletal-muscle enzyme assays.
    exposure
    Direct FAD addition; independent MCAD activity and immunoblot readouts.
    limitations
    Activity and abundance are related observations, not proof that protein loss is the only cause of incomplete rescue.
    nutrient_topic
    Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
    organism
    Mus musculus
    plain_language
    For MCAD, supplying cofactor alone could not promptly restore the missing enzyme capacity.
    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
    Skeletal-muscle homogenates
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 944–955

    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-mcad-rescue-limit FAD added to muscle assays only mildly improved depressed MCAD activity in Slc25a32 mutant mice; MCAD protein abundance was also lower in K235R homozygotes. Condition category: machinery_impairment nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: For MCAD, supplying cofactor alone could not promptly restore the missing enzyme capacity. organism: Mus musculus tissue_or_cell_type: Skeletal-muscle homogenates experimental_model: Slc25a32-null embryos and missense knock-in mice, isolated mitochondria and skeletal-muscle enzyme assays. limitations: Activity and abundance are related observations, not proof that protein loss is the only cause of incomplete rescue. exposure: Direct FAD addition; independent MCAD activity and immunoblot readouts. evidence_spans: [{"source_bundle": "artifacts/riboflavin_metabolism_sources.json", "source_key": "PMC11072207", "locator": "HTML article p", "paragraph_index": 50, "char_start": 0, "char_end": 1147, "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. Adding FAD directly to muscle enzyme assays fully restored the depressed SBCAD activity in the Slc25a32 mutant-mouse experiments.

    FAD → Mouse short/branched-chain acyl-CoA dehydrogenase / Acadsb source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Flavin supply supports a distinct branched-chain amino-acid oxidation step.
    evidence_spans
    [{"source_bundle": "artifacts/riboflavin_metabolism_sources.json", "source_key": "PMC11072207", "locator": "HTML article p", "paragraph_index": 50, "char_start": 0, "char_end": 1147, "evidence_access": "full-text"}]
    experimental_model
    Slc25a32-null embryos and missense knock-in mice, isolated mitochondria and skeletal-muscle enzyme assays.
    exposure
    FAD added directly to separate acyl-CoA dehydrogenase assays.
    limitations
    In vitro rescue differs from oral riboflavin response; the most pronounced enzyme defects occurred in K235R homozygotes.
    nutrient_topic
    Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
    organism
    Mus musculus
    plain_language
    One amino-acid oxidation enzyme retained activity that could be restored by adding its cofactor.
    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
    Skeletal-muscle homogenates
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 930–942

    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-sbcad-fad-rescue Adding FAD directly to muscle enzyme assays fully restored the depressed SBCAD activity in the Slc25a32 mutant-mouse experiments. Condition category: machinery_impairment nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: One amino-acid oxidation enzyme retained activity that could be restored by adding its cofactor. organism: Mus musculus tissue_or_cell_type: Skeletal-muscle homogenates experimental_model: Slc25a32-null embryos and missense knock-in mice, isolated mitochondria and skeletal-muscle enzyme assays. limitations: In vitro rescue differs from oral riboflavin response; the most pronounced enzyme defects occurred in K235R homozygotes. exposure: FAD added directly to separate acyl-CoA dehydrogenase assays. cross_nutrient: Flavin supply supports a distinct branched-chain amino-acid oxidation step. evidence_spans: [{"source_bundle": "artifacts/riboflavin_metabolism_sources.json", "source_key": "PMC11072207", "locator": "HTML article p", "paragraph_index": 50, "char_start": 0, "char_end": 1147, "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

  3. FAD added to muscle assays only mildly improved depressed VLCAD activity in Slc25a32 mutant mice; VLCAD abundance was lower in K235R homozygotes.

    FAD → Mouse very-long-chain acyl-CoA dehydrogenase / Acadvl source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_spans
    [{"source_bundle": "artifacts/riboflavin_metabolism_sources.json", "source_key": "PMC11072207", "locator": "HTML article p", "paragraph_index": 50, "char_start": 0, "char_end": 1147, "evidence_access": "full-text"}]
    experimental_model
    Slc25a32-null embryos and missense knock-in mice, isolated mitochondria and skeletal-muscle enzyme assays.
    exposure
    Direct FAD addition; VLCAD measured separately from MCAD.
    limitations
    This does not establish the response of genetic ACADVL disease to riboflavin.
    nutrient_topic
    Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
    organism
    Mus musculus
    plain_language
    The long-chain oxidation enzyme also had limitations beyond immediately available free cofactor.
    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
    Skeletal-muscle homogenates
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 957–968

    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-vlcad-rescue-limit FAD added to muscle assays only mildly improved depressed VLCAD activity in Slc25a32 mutant mice; VLCAD abundance was lower in K235R homozygotes. Condition category: machinery_impairment nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The long-chain oxidation enzyme also had limitations beyond immediately available free cofactor. organism: Mus musculus tissue_or_cell_type: Skeletal-muscle homogenates experimental_model: Slc25a32-null embryos and missense knock-in mice, isolated mitochondria and skeletal-muscle enzyme assays. limitations: This does not establish the response of genetic ACADVL disease to riboflavin. exposure: Direct FAD addition; VLCAD measured separately from MCAD. evidence_spans: [{"source_bundle": "artifacts/riboflavin_metabolism_sources.json", "source_key": "PMC11072207", "locator": "HTML article p", "paragraph_index": 50, "char_start": 0, "char_end": 1147, "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

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