Component

Mouse mitochondrial acyl carrier protein / Ndufab1

Mouse mitochondrial acyl carrier protein / Ndufab1. Identity is distinct from its gene and experimentally modified states; see each claim for organism and scope.

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. Cardiac Ndufab1 deletion reduced assembled respiratory complexes I–III and supercomplexes in mouse heart mitochondria.

    Mouse mitochondrial acyl carrier protein / Ndufab1 → Mitochondrial respiratory supercomplex assembly source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    true
    evidence_location
    Full text lines 49–55; Fig. 3; Supplementary Figs. S6–S10
    experimental_model
    Cardiomyocyte-specific Ndufab1 knockout mice and isolated heart mitochondria
    exposure
    Cardiac-specific genetic deletion; 6- and 16-week assembly assays, 6- and 10-week respiratory assays.
    limitations
    The FeS subunits of complexes II/III were preferentially affected, whereas broader complex-I subunit loss supports an additional assembly role. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
    nutrient_topic
    Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
    organism
    Mus musculus
    plain_language
    Loss of the carrier impaired assembly of several respiratory complexes in mouse heart.
    primary_references
    [b5-met-ndufab2019] NDUFAB1 confers cardio-protection by enhancing mitochondrial bioenergetics through coordination of respiratory complex and supercomplex assembly. (2019). https://pubmed.ncbi.nlm.nih.gov/31366990/ DOI: 10.1038/s41422-019-0208-x
    tissue_or_cell_type
    Heart mitochondria
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 949–961

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cardiomyocyte-specific Ndufab1 knockout mice and isolated heart mitochondria · source_derived_draft · unverified_draft

    ### b5-met-heart-acp-complex-assembly Cardiac Ndufab1 deletion reduced assembled respiratory complexes I–III and supercomplexes in mouse heart mitochondria. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Loss of the carrier impaired assembly of several respiratory complexes in mouse heart. organism: Mus musculus tissue_or_cell_type: Heart mitochondria experimental_model: Cardiomyocyte-specific Ndufab1 knockout mice and isolated heart mitochondria limitations: The FeS subunits of complexes II/III were preferentially affected, whereas broader complex-I subunit loss supports an additional assembly role. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: Cardiac-specific genetic deletion; 6- and 16-week assembly assays, 6- and 10-week respiratory assays. cross_nutrient: true evidence_location: Full text lines 49–55; Fig. 3; Supplementary Figs. S6–S10 [b5-met-ndufab2019] NDUFAB1 confers cardio-protection by enhancing mitochondrial bioenergetics through coordination of respiratory complex and supercomplex assembly. (2019). https://pubmed.ncbi.nlm.nih.gov/31366990/ DOI: 10.1038/s41422-019-0208-x
    Complete structured claim and evidence

  2. In the cardiac Ndufab1-knockout study, the measured mitochondrial protein lipoylation was not significantly changed despite respiratory defects.

    Mouse mitochondrial acyl carrier protein / Ndufab1 → Mitochondrial protein lipoylation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    true
    evidence_location
    Full text line 47; Supplementary Fig. S4B
    experimental_model
    Cardiomyocyte-specific Ndufab1 knockout mice and isolated heart mitochondria
    exposure
    Cardiomyocyte-specific Ndufab1 deletion.
    limitations
    A null result for these measurements is not proof that all fatty-acid synthesis was intact. Different tissue, developmental timing and depletion conditions preclude a same-context contradiction with HEK293T cells. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
    nutrient_topic
    Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
    organism
    Mus musculus
    plain_language
    Mouse heart respiratory failure occurred without the measured lipoylation defect seen in the cultured-cell study.
    primary_references
    [b5-met-ndufab2019] NDUFAB1 confers cardio-protection by enhancing mitochondrial bioenergetics through coordination of respiratory complex and supercomplex assembly. (2019). https://pubmed.ncbi.nlm.nih.gov/31366990/ DOI: 10.1038/s41422-019-0208-x
    tissue_or_cell_type
    Heart mitochondria
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 977–989

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cardiomyocyte-specific Ndufab1 knockout mice and isolated heart mitochondria · source_derived_draft · unverified_draft

    ### b5-met-heart-acp-lipoylation-spared In the cardiac Ndufab1-knockout study, the measured mitochondrial protein lipoylation was not significantly changed despite respiratory defects. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Mouse heart respiratory failure occurred without the measured lipoylation defect seen in the cultured-cell study. organism: Mus musculus tissue_or_cell_type: Heart mitochondria experimental_model: Cardiomyocyte-specific Ndufab1 knockout mice and isolated heart mitochondria limitations: A null result for these measurements is not proof that all fatty-acid synthesis was intact. Different tissue, developmental timing and depletion conditions preclude a same-context contradiction with HEK293T cells. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: Cardiomyocyte-specific Ndufab1 deletion. cross_nutrient: true evidence_location: Full text line 47; Supplementary Fig. S4B [b5-met-ndufab2019] NDUFAB1 confers cardio-protection by enhancing mitochondrial bioenergetics through coordination of respiratory complex and supercomplex assembly. (2019). https://pubmed.ncbi.nlm.nih.gov/31366990/ DOI: 10.1038/s41422-019-0208-x
    Complete structured claim and evidence

  3. Cardiac Ndufab1 deletion lowered oxygen consumption supported by complex I-, II-, or III-linked substrates, while complex IV-linked respiration remained unchanged.

    Mouse mitochondrial acyl carrier protein / Ndufab1 → ADP-stimulated 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 lines 47–49; Fig. 3A
    experimental_model
    Cardiomyocyte-specific Ndufab1 knockout mice and isolated heart mitochondria
    exposure
    Cardiac-specific genetic deletion; 6- and 16-week assembly assays, 6- and 10-week respiratory assays.
    limitations
    Isolated-mitochondria oxygen consumption does not measure nutrient absorption or human exercise capacity. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
    nutrient_topic
    Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
    organism
    Mus musculus
    plain_language
    The respiratory defect affected several upstream electron-transfer routes but spared the tested complex IV route.
    primary_references
    [b5-met-ndufab2019] NDUFAB1 confers cardio-protection by enhancing mitochondrial bioenergetics through coordination of respiratory complex and supercomplex assembly. (2019). https://pubmed.ncbi.nlm.nih.gov/31366990/ DOI: 10.1038/s41422-019-0208-x
    tissue_or_cell_type
    Heart mitochondria
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 963–975

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cardiomyocyte-specific Ndufab1 knockout mice and isolated heart mitochondria · source_derived_draft · unverified_draft

    ### b5-met-heart-acp-respiration Cardiac Ndufab1 deletion lowered oxygen consumption supported by complex I-, II-, or III-linked substrates, while complex IV-linked respiration remained unchanged. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The respiratory defect affected several upstream electron-transfer routes but spared the tested complex IV route. organism: Mus musculus tissue_or_cell_type: Heart mitochondria experimental_model: Cardiomyocyte-specific Ndufab1 knockout mice and isolated heart mitochondria limitations: Isolated-mitochondria oxygen consumption does not measure nutrient absorption or human exercise capacity. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: Cardiac-specific genetic deletion; 6- and 16-week assembly assays, 6- and 10-week respiratory assays. cross_nutrient: false evidence_location: Full text lines 47–49; Fig. 3A [b5-met-ndufab2019] NDUFAB1 confers cardio-protection by enhancing mitochondrial bioenergetics through coordination of respiratory complex and supercomplex assembly. (2019). https://pubmed.ncbi.nlm.nih.gov/31366990/ DOI: 10.1038/s41422-019-0208-x
    Complete structured claim and evidence

  4. Ndufab1 siRNA in mouse C2C12 myoblasts reduced mitochondrial Nfs1, Isd11 and Iscu2 protein abundance.

    Mouse mitochondrial acyl carrier protein / Ndufab1 → Mouse cysteine desulfurase / Nfs1 source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    true
    evidence_location
    Full text line 117; Fig. 3C
    experimental_model
    Pooled Ndufab1 siRNA versus scrambled control
    exposure
    Ndufab1-targeting siRNA; immunoblot of isolated mitochondria.
    limitations
    The mammalian intact Nfs1–Isd11 complex could not be resolved by the authors with BN-PAGE; the direct mammalian result is subunit abundance. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
    nutrient_topic
    Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
    organism
    Mus musculus
    plain_language
    The iron–sulfur machinery also became less stable after carrier depletion in mouse muscle cells.
    primary_references
    [b5-met-acp2016] The mitochondrial acyl carrier protein (ACP) coordinates mitochondrial fatty acid synthesis with iron sulfur cluster biogenesis. (2016). https://pubmed.ncbi.nlm.nih.gov/27540631/ DOI: 10.7554/elife.17828
    tissue_or_cell_type
    C2C12 myoblast mitochondria
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 921–933

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Pooled Ndufab1 siRNA versus scrambled control · source_derived_draft · unverified_draft

    ### b5-met-mouse-acp-isu-stability Ndufab1 siRNA in mouse C2C12 myoblasts reduced mitochondrial Nfs1, Isd11 and Iscu2 protein abundance. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The iron–sulfur machinery also became less stable after carrier depletion in mouse muscle cells. organism: Mus musculus tissue_or_cell_type: C2C12 myoblast mitochondria experimental_model: Pooled Ndufab1 siRNA versus scrambled control limitations: The mammalian intact Nfs1–Isd11 complex could not be resolved by the authors with BN-PAGE; the direct mammalian result is subunit abundance. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: Ndufab1-targeting siRNA; immunoblot of isolated mitochondria. cross_nutrient: true evidence_location: Full text line 117; Fig. 3C [b5-met-acp2016] The mitochondrial acyl carrier protein (ACP) coordinates mitochondrial fatty acid synthesis with iron sulfur cluster biogenesis. (2016). https://pubmed.ncbi.nlm.nih.gov/27540631/ DOI: 10.7554/elife.17828
    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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