Component

MMUT gene (Homo sapiens)

MMUT gene (Homo sapiens)

6 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. MMUT knockout reduced propionate-derived protein labeling about sixfold in HFF1 human fibroblasts.

    MMUT gene (Homo sapiens) → Propionate-derived carbon incorporation into cellular protein source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    evidence_location
    Full text Results; Figure 2C,E
    experimental_model
    HFF1 human fibroblasts with two CRISPR guides
    exposure
    MMUT CRISPR knockout versus OR7G3 guide control; [14C]propionate
    limitations
    Protein labeling integrates metabolism and protein synthesis; not direct MMUT flux.
    nutrient_topic
    Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
    organism
    Homo sapiens
    plain_language
    These human fibroblasts relied strongly on MMUT for the measured use of propionate carbon.
    primary_references
    [2024-propionate-cell-dependence] Differential utilization of vitamin B12-dependent and independent pathways for propionate metabolism across human cells. (2024). https://pubmed.ncbi.nlm.nih.gov/39128713/ DOI: 10.1016/j.jbc.2024.107662
    tissue_or_cell_type
    Foreskin fibroblasts
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1300–1312

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · HFF1 human fibroblasts with two CRISPR guides · source_derived_draft · unverified_draft

    ### hff1-mmut-ko-lowers-propionate-label MMUT knockout reduced propionate-derived protein labeling about sixfold in HFF1 human fibroblasts. Condition category: machinery_impairment nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: These human fibroblasts relied strongly on MMUT for the measured use of propionate carbon. organism: Homo sapiens tissue_or_cell_type: Foreskin fibroblasts experimental_model: HFF1 human fibroblasts with two CRISPR guides limitations: Protein labeling integrates metabolism and protein synthesis; not direct MMUT flux. exposure: MMUT CRISPR knockout versus OR7G3 guide control; [14C]propionate cross_nutrient: false evidence_location: Full text Results; Figure 2C,E [2024-propionate-cell-dependence] Differential utilization of vitamin B12-dependent and independent pathways for propionate metabolism across human cells. (2024). https://pubmed.ncbi.nlm.nih.gov/39128713/ DOI: 10.1016/j.jbc.2024.107662
    Complete structured claim and evidence

  2. MMUT knockout did not reduce propionate-derived protein labeling in HT-29 colorectal cancer cells.

    MMUT gene (Homo sapiens) → Propionate-derived carbon incorporation into cellular protein source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    evidence_location
    Full text Results; Figure 2C,E
    experimental_model
    HT-29 human colorectal adenocarcinoma cells
    exposure
    MMUT CRISPR knockout versus OR7G3 guide control; [14C]propionate
    limitations
    Transformed cell line; does not establish pathway proportions in normal human colon.
    nutrient_topic
    Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
    organism
    Homo sapiens
    plain_language
    This human cancer cell line retained propionate use without MMUT, unlike the tested fibroblasts.
    primary_references
    [2024-propionate-cell-dependence] Differential utilization of vitamin B12-dependent and independent pathways for propionate metabolism across human cells. (2024). https://pubmed.ncbi.nlm.nih.gov/39128713/ DOI: 10.1016/j.jbc.2024.107662
    tissue_or_cell_type
    Colorectal adenocarcinoma cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1314–1326

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · HT-29 human colorectal adenocarcinoma cells · source_derived_draft · unverified_draft

    ### ht29-mmut-ko-preserves-propionate-label MMUT knockout did not reduce propionate-derived protein labeling in HT-29 colorectal cancer cells. Condition category: machinery_impairment nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: This human cancer cell line retained propionate use without MMUT, unlike the tested fibroblasts. organism: Homo sapiens tissue_or_cell_type: Colorectal adenocarcinoma cells experimental_model: HT-29 human colorectal adenocarcinoma cells limitations: Transformed cell line; does not establish pathway proportions in normal human colon. exposure: MMUT CRISPR knockout versus OR7G3 guide control; [14C]propionate cross_nutrient: false evidence_location: Full text Results; Figure 2C,E [2024-propionate-cell-dependence] Differential utilization of vitamin B12-dependent and independent pathways for propionate metabolism across human cells. (2024). https://pubmed.ncbi.nlm.nih.gov/39128713/ DOI: 10.1016/j.jbc.2024.107662
    Complete structured claim and evidence

  3. MMUT-deficient human kidney cells failed to show the control mt-Keima lysosomal shift after 24 hours of 5 micromolar rotenone.

    MMUT gene (Homo sapiens) → Mitochondrial delivery to lysosomes source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    evidence_location
    Full text Results; Figures 2f,5c-f,6c-d
    experimental_model
    Urine-derived human mut0 MMA kidney tubular cells
    exposure
    MMUT-inactivating genotypes plus 5 micromolar rotenone for 24 hours
    limitations
    Inherited MMUT machinery defect; cannot be generalized to nutritional B12 deficiency or neurons. mt-Keima is a delivery reporter.
    nutrient_topic
    Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
    organism
    Homo sapiens
    plain_language
    After experimental mitochondrial damage, these patient kidney cells delivered fewer mitochondria to lysosomes.
    primary_references
    [luciani-2020-mmut-mitophagy] Impaired mitophagy links mitochondrial disease to epithelial stress in methylmalonyl-CoA mutase deficiency. (2020). https://pubmed.ncbi.nlm.nih.gov/32080200/ DOI: 10.1038/s41467-020-14729-8
    tissue_or_cell_type
    Kidney tubular cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1342–1354

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Urine-derived human mut0 MMA kidney tubular cells · source_derived_draft · unverified_draft

    ### mut0-kidney-impaired-mito-delivery MMUT-deficient human kidney cells failed to show the control mt-Keima lysosomal shift after 24 hours of 5 micromolar rotenone. Condition category: machinery_impairment nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: After experimental mitochondrial damage, these patient kidney cells delivered fewer mitochondria to lysosomes. organism: Homo sapiens tissue_or_cell_type: Kidney tubular cells experimental_model: Urine-derived human mut0 MMA kidney tubular cells limitations: Inherited MMUT machinery defect; cannot be generalized to nutritional B12 deficiency or neurons. mt-Keima is a delivery reporter. exposure: MMUT-inactivating genotypes plus 5 micromolar rotenone for 24 hours cross_nutrient: false evidence_location: Full text Results; Figures 2f,5c-f,6c-d [luciani-2020-mmut-mitophagy] Impaired mitophagy links mitochondrial disease to epithelial stress in methylmalonyl-CoA mutase deficiency. (2020). https://pubmed.ncbi.nlm.nih.gov/32080200/ DOI: 10.1038/s41467-020-14729-8
    Complete structured claim and evidence

  4. MMUT-deficient human kidney cells showed reduced Parkin recruitment after 5 micromolar rotenone for four hours.

    MMUT gene (Homo sapiens) → Parkin recruitment to mitochondria source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    evidence_location
    Full text Results; Figures 2f,5c-f,6c-d
    experimental_model
    Urine-derived human mut0 MMA kidney tubular cells
    exposure
    MMUT-inactivating genotypes plus 5 micromolar rotenone for four hours
    limitations
    Inherited MMUT machinery defect; cannot be generalized to nutritional B12 deficiency or neurons. Endogenous PINK1 was not directly quantified.
    nutrient_topic
    Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
    organism
    Homo sapiens
    plain_language
    In this damage assay, patient kidney cells marked fewer mitochondria with Parkin.
    primary_references
    [luciani-2020-mmut-mitophagy] Impaired mitophagy links mitochondrial disease to epithelial stress in methylmalonyl-CoA mutase deficiency. (2020). https://pubmed.ncbi.nlm.nih.gov/32080200/ DOI: 10.1038/s41467-020-14729-8
    tissue_or_cell_type
    Kidney tubular cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1356–1368

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Urine-derived human mut0 MMA kidney tubular cells · source_derived_draft · unverified_draft

    ### mut0-kidney-parkin-recruitment MMUT-deficient human kidney cells showed reduced Parkin recruitment after 5 micromolar rotenone for four hours. Condition category: machinery_impairment nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: In this damage assay, patient kidney cells marked fewer mitochondria with Parkin. organism: Homo sapiens tissue_or_cell_type: Kidney tubular cells experimental_model: Urine-derived human mut0 MMA kidney tubular cells limitations: Inherited MMUT machinery defect; cannot be generalized to nutritional B12 deficiency or neurons. Endogenous PINK1 was not directly quantified. exposure: MMUT-inactivating genotypes plus 5 micromolar rotenone for four hours cross_nutrient: false evidence_location: Full text Results; Figures 2f,5c-f,6c-d [luciani-2020-mmut-mitophagy] Impaired mitophagy links mitochondrial disease to epithelial stress in methylmalonyl-CoA mutase deficiency. (2020). https://pubmed.ncbi.nlm.nih.gov/32080200/ DOI: 10.1038/s41467-020-14729-8
    Complete structured claim and evidence

  5. Human mut0 MMA kidney tubular cells had lower basal oxygen consumption than control cells.

    MMUT gene (Homo sapiens) → Basal mitochondrial oxygen consumption source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    evidence_location
    Full text Results; Figures 2f,5c-f,6c-d
    experimental_model
    Urine-derived human mut0 MMA kidney tubular cells
    exposure
    Patient MMUT-inactivating genotypes versus controls
    limitations
    Inherited MMUT machinery defect; cannot be generalized to nutritional B12 deficiency or neurons.
    nutrient_topic
    Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
    organism
    Homo sapiens
    plain_language
    Kidney cells from these patients with MMUT defects consumed less oxygen in the basal assay.
    primary_references
    [luciani-2020-mmut-mitophagy] Impaired mitophagy links mitochondrial disease to epithelial stress in methylmalonyl-CoA mutase deficiency. (2020). https://pubmed.ncbi.nlm.nih.gov/32080200/ DOI: 10.1038/s41467-020-14729-8
    tissue_or_cell_type
    Kidney tubular cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1328–1340

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Urine-derived human mut0 MMA kidney tubular cells · source_derived_draft · unverified_draft

    ### mut0-kidney-reduced-respiration Human mut0 MMA kidney tubular cells had lower basal oxygen consumption than control cells. Condition category: machinery_impairment nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Kidney cells from these patients with MMUT defects consumed less oxygen in the basal assay. organism: Homo sapiens tissue_or_cell_type: Kidney tubular cells experimental_model: Urine-derived human mut0 MMA kidney tubular cells limitations: Inherited MMUT machinery defect; cannot be generalized to nutritional B12 deficiency or neurons. exposure: Patient MMUT-inactivating genotypes versus controls cross_nutrient: false evidence_location: Full text Results; Figures 2f,5c-f,6c-d [luciani-2020-mmut-mitophagy] Impaired mitophagy links mitochondrial disease to epithelial stress in methylmalonyl-CoA mutase deficiency. (2020). https://pubmed.ncbi.nlm.nih.gov/32080200/ DOI: 10.1038/s41467-020-14729-8
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Adenoviral human PINK1 expression restored Parkin recruitment in MMUT-deficient human kidney tubular cells.

    Human PINK1 kinase → Parkin recruitment to mitochondria source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    evidence_location
    Full text Results; Figures 2f,5c-f,6c-d
    experimental_model
    Urine-derived human mut0 MMA kidney tubular cells
    exposure
    HA-PINK1 adenovirus versus empty-vector control
    limitations
    Inherited MMUT machinery defect; cannot be generalized to nutritional B12 deficiency or neurons. Gene-delivery rescue is not an established clinical therapy.
    nutrient_topic
    Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
    organism
    Homo sapiens
    plain_language
    Adding PINK1 restored mitochondrial marking in this patient-cell model.
    primary_references
    [luciani-2020-mmut-mitophagy] Impaired mitophagy links mitochondrial disease to epithelial stress in methylmalonyl-CoA mutase deficiency. (2020). https://pubmed.ncbi.nlm.nih.gov/32080200/ DOI: 10.1038/s41467-020-14729-8
    tissue_or_cell_type
    Kidney tubular cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1370–1382

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Urine-derived human mut0 MMA kidney tubular cells · source_derived_draft · unverified_draft

    ### pink1-restores-parkin-mmut-kidney Adenoviral human PINK1 expression restored Parkin recruitment in MMUT-deficient human kidney tubular cells. Condition category: machinery_impairment nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Adding PINK1 restored mitochondrial marking in this patient-cell model. organism: Homo sapiens tissue_or_cell_type: Kidney tubular cells experimental_model: Urine-derived human mut0 MMA kidney tubular cells limitations: Inherited MMUT machinery defect; cannot be generalized to nutritional B12 deficiency or neurons. Gene-delivery rescue is not an established clinical therapy. exposure: HA-PINK1 adenovirus versus empty-vector control cross_nutrient: false evidence_location: Full text Results; Figures 2f,5c-f,6c-d [luciani-2020-mmut-mitophagy] Impaired mitophagy links mitochondrial disease to epithelial stress in methylmalonyl-CoA mutase deficiency. (2020). https://pubmed.ncbi.nlm.nih.gov/32080200/ DOI: 10.1038/s41467-020-14729-8
    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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