Component

Human mitochondrial acyl carrier protein / NDUFAB1

Human 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. Mitochondrial ACP knockdown in HEK293T cells subsequently reduced respiratory complex I specific activity.

    Human mitochondrial acyl carrier protein / NDUFAB1 → Mitochondrial respiratory complex I source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    evidence_location
    Abstract, later phenotypic changes
    experimental_model
    Mitochondrial ACP siRNA in HEK293T cells
    exposure
    ACP mRNA and protein reduced by more than 85% within 24 hours; later measurements followed knockdown.
    limitations
    Temporal ordering alone does not separate all direct complex-I effects from secondary cellular injury; abstract-level extraction. 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
    Homo sapiens
    plain_language
    The carrier-protein defect also impaired complex I function.
    primary_references
    [b5-met-acp2009] Down-regulation of mitochondrial acyl carrier protein in mammalian cells compromises protein lipoylation and respiratory complex I and results in cell death. (2009). https://pubmed.ncbi.nlm.nih.gov/19221180/ DOI: 10.1074/jbc.m806991200
    tissue_or_cell_type
    HEK293T mitochondria
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 837–849

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mitochondrial ACP siRNA in HEK293T cells · source_derived_draft · unverified_draft

    ### b5-met-mtacp-complex-i Mitochondrial ACP knockdown in HEK293T cells subsequently reduced respiratory complex I specific activity. 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 carrier-protein defect also impaired complex I function. organism: Homo sapiens tissue_or_cell_type: HEK293T mitochondria experimental_model: Mitochondrial ACP siRNA in HEK293T cells limitations: Temporal ordering alone does not separate all direct complex-I effects from secondary cellular injury; abstract-level extraction. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: ACP mRNA and protein reduced by more than 85% within 24 hours; later measurements followed knockdown. cross_nutrient: false evidence_location: Abstract, later phenotypic changes [b5-met-acp2009] Down-regulation of mitochondrial acyl carrier protein in mammalian cells compromises protein lipoylation and respiratory complex I and results in cell death. (2009). https://pubmed.ncbi.nlm.nih.gov/19221180/ DOI: 10.1074/jbc.m806991200
    Complete structured claim and evidence

  2. Mitochondrial ACP knockdown in HEK293T cells reduced the proportion of mitochondrial proteins recognized as lipoylated before later respiratory defects.

    Human 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
    Abstract, earliest phenotypic changes; Fig. 2 caption
    experimental_model
    Mitochondrial ACP siRNA in HEK293T cells
    exposure
    ACP mRNA and protein reduced by more than 85% within 24 hours; later measurements followed knockdown.
    limitations
    Antibody-based lipoylation readout; not a measurement of dietary lipoic acid or pantothenate shortage. 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
    Homo sapiens
    plain_language
    Loss of the mitochondrial carrier impaired attachment of the lipoate cofactor to proteins.
    primary_references
    [b5-met-acp2009] Down-regulation of mitochondrial acyl carrier protein in mammalian cells compromises protein lipoylation and respiratory complex I and results in cell death. (2009). https://pubmed.ncbi.nlm.nih.gov/19221180/ DOI: 10.1074/jbc.m806991200
    tissue_or_cell_type
    HEK293T mitochondrial proteins
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 823–835

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mitochondrial ACP siRNA in HEK293T cells · source_derived_draft · unverified_draft

    ### b5-met-mtacp-lipoylation Mitochondrial ACP knockdown in HEK293T cells reduced the proportion of mitochondrial proteins recognized as lipoylated before later 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: Loss of the mitochondrial carrier impaired attachment of the lipoate cofactor to proteins. organism: Homo sapiens tissue_or_cell_type: HEK293T mitochondrial proteins experimental_model: Mitochondrial ACP siRNA in HEK293T cells limitations: Antibody-based lipoylation readout; not a measurement of dietary lipoic acid or pantothenate shortage. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: ACP mRNA and protein reduced by more than 85% within 24 hours; later measurements followed knockdown. cross_nutrient: true evidence_location: Abstract, earliest phenotypic changes; Fig. 2 caption [b5-met-acp2009] Down-regulation of mitochondrial acyl carrier protein in mammalian cells compromises protein lipoylation and respiratory complex I and results in cell death. (2009). https://pubmed.ncbi.nlm.nih.gov/19221180/ DOI: 10.1074/jbc.m806991200
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Human AASDHPPT transfers the CoA-derived 4′-phosphopantetheine group to a conserved serine in human mitochondrial ACP.

    Coenzyme A → Human phosphopantetheinylated mitochondrial ACP source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    evidence_location
    Abstract, substrate-specificity result
    experimental_model
    Recombinant human transferase and mitochondrial ACP substrate
    exposure
    Enzymatic transfer from CoA; no dietary intervention.
    limitations
    The experiment establishes substrate competence, not the in-vivo location of the transfer reaction. 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
    Homo sapiens
    plain_language
    The mitochondrial carrier protein also needs a chemical arm derived from CoA.
    primary_references
    [b5-met-joshi2003] Cloning, expression, and characterization of a human 4'-phosphopantetheinyl transferase with broad substrate specificity. (2003). https://pubmed.ncbi.nlm.nih.gov/12815048/ DOI: 10.1074/jbc.m305459200
    tissue_or_cell_type
    Mitochondrial ACP substrate; in-vitro reaction

    Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 809–821

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human transferase and mitochondrial ACP substrate · source_derived_draft · unverified_draft

    ### b5-met-aasdhppt-mtacp Human AASDHPPT transfers the CoA-derived 4′-phosphopantetheine group to a conserved serine in human mitochondrial ACP. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The mitochondrial carrier protein also needs a chemical arm derived from CoA. organism: Homo sapiens tissue_or_cell_type: Mitochondrial ACP substrate; in-vitro reaction experimental_model: Recombinant human transferase and mitochondrial ACP substrate limitations: The experiment establishes substrate competence, not the in-vivo location of the transfer reaction. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: Enzymatic transfer from CoA; no dietary intervention. cross_nutrient: false evidence_location: Abstract, substrate-specificity result [b5-met-joshi2003] Cloning, expression, and characterization of a human 4'-phosphopantetheinyl transferase with broad substrate specificity. (2003). https://pubmed.ncbi.nlm.nih.gov/12815048/ DOI: 10.1074/jbc.m305459200
    Complete structured claim and evidence

  2. Adding lipoic acid to the culture medium did not reverse the protein-lipoylation defect caused by mitochondrial ACP knockdown in HEK293T cells.

    Lipoic acid → Mitochondrial protein lipoylation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    true
    evidence_location
    Abstract, lipoic-acid supplementation result
    experimental_model
    Mitochondrial ACP siRNA in HEK293T cells
    exposure
    Lipoic-acid supplementation of ACP-knockdown cultures; concentration not extracted.
    limitations
    Lipoic acid offered some oxidative-damage protection, but that is a different endpoint; result is not a universal statement about every lipoylation disorder. 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
    Homo sapiens
    plain_language
    External lipoic acid did not bypass this carrier-protein defect.
    primary_references
    [b5-met-acp2009] Down-regulation of mitochondrial acyl carrier protein in mammalian cells compromises protein lipoylation and respiratory complex I and results in cell death. (2009). https://pubmed.ncbi.nlm.nih.gov/19221180/ DOI: 10.1074/jbc.m806991200
    tissue_or_cell_type
    HEK293T cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 851–863

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mitochondrial ACP siRNA in HEK293T cells · source_derived_draft · unverified_draft

    ### b5-met-lipoate-nonrescue Adding lipoic acid to the culture medium did not reverse the protein-lipoylation defect caused by mitochondrial ACP knockdown in HEK293T cells. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: External lipoic acid did not bypass this carrier-protein defect. organism: Homo sapiens tissue_or_cell_type: HEK293T cells experimental_model: Mitochondrial ACP siRNA in HEK293T cells limitations: Lipoic acid offered some oxidative-damage protection, but that is a different endpoint; result is not a universal statement about every lipoylation disorder. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: Lipoic-acid supplementation of ACP-knockdown cultures; concentration not extracted. cross_nutrient: true evidence_location: Abstract, lipoic-acid supplementation result [b5-met-acp2009] Down-regulation of mitochondrial acyl carrier protein in mammalian cells compromises protein lipoylation and respiratory complex I and results in cell death. (2009). https://pubmed.ncbi.nlm.nih.gov/19221180/ DOI: 10.1074/jbc.m806991200
    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