Component

Human pantothenate kinase 2 / PANK2

Human pantothenate kinase 2 / PANK2. See linked evidence for experiment-specific scope. Human pantothenate kinase 2.

7 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. Human PANK2 was mitochondrial whereas mouse Pank2 localized to the cytosol in the comparative study.

    Human pantothenate kinase 2 / PANK2 → Mouse pantothenate kinase 2 / Pank2 source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Comparative human and mouse PANK2 biochemistry and cellular localization
    exposure
    Comparative localization of human and mouse proteins; exact constructs/cell lines not extracted.
    limitations
    Localization difference must be retained when translating mouse knockout or rescue findings; this claim does not assign human PANK2 to a particular mitochondrial subcompartment.
    nutrient_topic
    Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
    organism
    Homo sapiens and Mus musculus
    plain_language
    The mouse Pank2 model differs from humans in where the enzyme resides.
    primary_references
    [b5-bio-pank2mouse] Localization and regulation of mouse pantothenate kinase 2. (2007). https://pubmed.ncbi.nlm.nih.gov/17825826/ DOI: 10.1016/j.febslet.2007.08.056
    tissue_or_cell_type
    Cellular subcellular-localization experiments

    Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 639–650

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Comparative human and mouse PANK2 biochemistry and cellular localization · source_derived_draft · unverified_draft

    ### b5-bio-pank2-species-localization Human PANK2 was mitochondrial whereas mouse Pank2 localized to the cytosol in the comparative study. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The mouse Pank2 model differs from humans in where the enzyme resides. organism: Homo sapiens and Mus musculus tissue_or_cell_type: Cellular subcellular-localization experiments experimental_model: Comparative human and mouse PANK2 biochemistry and cellular localization limitations: Localization difference must be retained when translating mouse knockout or rescue findings; this claim does not assign human PANK2 to a particular mitochondrial subcompartment. exposure: Comparative localization of human and mouse proteins; exact constructs/cell lines not extracted. cross_nutrient: false [b5-bio-pank2mouse] Localization and regulation of mouse pantothenate kinase 2. (2007). https://pubmed.ncbi.nlm.nih.gov/17825826/ DOI: 10.1016/j.febslet.2007.08.056
    Complete structured claim and evidence

What acts on it

  1. Acetyl-CoA inhibited purified human PANK2 competitively with ATP; PANK2 inhibition was submicromolar in the reported preparations.

    Acetyl-CoA → Human pantothenate kinase 2 / PANK2 source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Human PANK2 in 293T-cell lysates and purified enzyme assays
    exposure
    293T-cell-lysate inhibition IC50 was 0.3 micromolar acetyl-CoA; purified-enzyme assays established ATP competition.
    limitations
    The lysate IC50 is preparation-specific and is not a intracellular or dietary adequacy threshold. Purified-enzyme competition and lysate potency are separately identified.
    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
    An existing CoA derivative feeds back to restrain PANK2.
    primary_references
    [b5-bio-pank2reg] Activation of human mitochondrial pantothenate kinase 2 by palmitoylcarnitine. (2007). https://pubmed.ncbi.nlm.nih.gov/17242360/ DOI: 10.1073/pnas.0607621104
    tissue_or_cell_type
    Purified recombinant protein; no intact tissue

    Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 600–611

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human PANK2 in 293T-cell lysates and purified enzyme assays · source_derived_draft · unverified_draft

    ### b5-bio-pank2-acetyl-inhibition Acetyl-CoA inhibited purified human PANK2 competitively with ATP; PANK2 inhibition was submicromolar in the reported preparations. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: An existing CoA derivative feeds back to restrain PANK2. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Human PANK2 in 293T-cell lysates and purified enzyme assays limitations: The lysate IC50 is preparation-specific and is not a intracellular or dietary adequacy threshold. Purified-enzyme competition and lysate potency are separately identified. exposure: 293T-cell-lysate inhibition IC50 was 0.3 micromolar acetyl-CoA; purified-enzyme assays established ATP competition. cross_nutrient: false [b5-bio-pank2reg] Activation of human mitochondrial pantothenate kinase 2 by palmitoylcarnitine. (2007). https://pubmed.ncbi.nlm.nih.gov/17242360/ DOI: 10.1073/pnas.0607621104
    Complete structured claim and evidence

  2. Free carnitine did not activate purified human PANK2 in the experiment shown in Fig. 4B.

    L-Carnitine → Human pantothenate kinase 2 / PANK2 source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    true
    experimental_model
    Human PANK2 in 293T-cell lysates and purified enzyme assays
    exposure
    Primary Fig. 4B purified-enzyme assay; carnitine concentration range not extracted.
    limitations
    The same paper observed free-carnitine activation in lysate preparations at higher concentrations, so the purified-enzyme negative result must not be generalized to every lysate condition. Neither assay tests clinical carnitine 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 purified enzyme did not respond directly to free carnitine.
    primary_references
    [b5-bio-pank2reg] Activation of human mitochondrial pantothenate kinase 2 by palmitoylcarnitine. (2007). https://pubmed.ncbi.nlm.nih.gov/17242360/ DOI: 10.1073/pnas.0607621104
    tissue_or_cell_type
    Purified recombinant protein; no intact tissue

    Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 626–637

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human PANK2 in 293T-cell lysates and purified enzyme assays · source_derived_draft · unverified_draft

    ### b5-bio-pank2-free-carnitine Free carnitine did not activate purified human PANK2 in the experiment shown in Fig. 4B. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The purified enzyme did not respond directly to free carnitine. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Human PANK2 in 293T-cell lysates and purified enzyme assays limitations: The same paper observed free-carnitine activation in lysate preparations at higher concentrations, so the purified-enzyme negative result must not be generalized to every lysate condition. Neither assay tests clinical carnitine supplementation. exposure: Primary Fig. 4B purified-enzyme assay; carnitine concentration range not extracted. cross_nutrient: true [b5-bio-pank2reg] Activation of human mitochondrial pantothenate kinase 2 by palmitoylcarnitine. (2007). https://pubmed.ncbi.nlm.nih.gov/17242360/ DOI: 10.1073/pnas.0607621104
    Complete structured claim and evidence

  3. Palmitoylcarnitine antagonized acetyl-CoA inhibition of human PANK2, providing a positive regulatory input in biochemical assays.

    Palmitoyl-L-carnitine → Human pantothenate kinase 2 / PANK2 source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    true
    experimental_model
    Human PANK2 in 293T-cell lysates and purified enzyme assays
    exposure
    Human PANK2 in 293T lysates and purified-enzyme assays; indexed Fig. 1 used 0.2 micromolar acetyl-CoA.
    limitations
    Acylcarnitine is a specific molecule; this does not show that free-carnitine supplements activate PANK2 in people. Intact-organism fatty-acid-demand interpretation was proposed.
    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
    A long-chain acylcarnitine can release the brake on PANK2.
    primary_references
    [b5-bio-pank2reg] Activation of human mitochondrial pantothenate kinase 2 by palmitoylcarnitine. (2007). https://pubmed.ncbi.nlm.nih.gov/17242360/ DOI: 10.1073/pnas.0607621104
    tissue_or_cell_type
    Purified recombinant protein; no intact tissue

    Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 613–624

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human PANK2 in 293T-cell lysates and purified enzyme assays · source_derived_draft · unverified_draft

    ### b5-bio-pank2-palmitoylcarnitine Palmitoylcarnitine antagonized acetyl-CoA inhibition of human PANK2, providing a positive regulatory input in biochemical assays. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: A long-chain acylcarnitine can release the brake on PANK2. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Human PANK2 in 293T-cell lysates and purified enzyme assays limitations: Acylcarnitine is a specific molecule; this does not show that free-carnitine supplements activate PANK2 in people. Intact-organism fatty-acid-demand interpretation was proposed. exposure: Human PANK2 in 293T lysates and purified-enzyme assays; indexed Fig. 1 used 0.2 micromolar acetyl-CoA. cross_nutrient: true [b5-bio-pank2reg] Activation of human mitochondrial pantothenate kinase 2 by palmitoylcarnitine. (2007). https://pubmed.ncbi.nlm.nih.gov/17242360/ DOI: 10.1073/pnas.0607621104
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. The gene-discovery study identified recessive PANK2 defects as the cause of the studied inherited neurodegeneration with brain iron accumulation.

    Human biallelic pathogenic PANK2 genotypes → Pantothenate kinase-associated neurodegeneration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Human recessive neurodegeneration gene-discovery study
    exposure
    Inherited recessive PANK2 defects; not a controlled vitamin-B5 depletion.
    limitations
    Primary gene-discovery abstract; proposed oxidative-stress mechanisms are not imported as proven consequences. No evidence here that pantothenate supplementation repairs the genetic lesion.
    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
    Inherited damage to a B5-using enzyme can cause disease even without low dietary B5.
    primary_references
    [b5-bio-pank2gene] A novel pantothenate kinase gene (PANK2) is defective in Hallervorden-Spatz syndrome. (2001). https://pubmed.ncbi.nlm.nih.gov/11479594/ DOI: 10.1038/ng572
    tissue_or_cell_type
    Human neurological disease and genetic analysis
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 717–728

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human recessive neurodegeneration gene-discovery study · source_derived_draft · unverified_draft

    ### b5-bio-pank2-genetic-disease The gene-discovery study identified recessive PANK2 defects as the cause of the studied inherited neurodegeneration with brain iron accumulation. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Inherited damage to a B5-using enzyme can cause disease even without low dietary B5. organism: Homo sapiens tissue_or_cell_type: Human neurological disease and genetic analysis experimental_model: Human recessive neurodegeneration gene-discovery study limitations: Primary gene-discovery abstract; proposed oxidative-stress mechanisms are not imported as proven consequences. No evidence here that pantothenate supplementation repairs the genetic lesion. exposure: Inherited recessive PANK2 defects; not a controlled vitamin-B5 depletion. cross_nutrient: false [b5-bio-pank2gene] A novel pantothenate kinase gene (PANK2) is defective in Hallervorden-Spatz syndrome. (2001). https://pubmed.ncbi.nlm.nih.gov/11479594/ DOI: 10.1038/ng572
    Complete structured claim and evidence

  2. FORT found no significant difference in 24-week PKAN-ADL change between fosmetpantotenate and placebo: adjusted difference −0.09 points, 95% CI −1.69 to 1.51, P=0.9115.

    Fosmetpantotenate → PKAN activities-of-daily-living score source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    evidence_location
    Full primary BioC Methods, Results and Discussion.
    experimental_model
    FORT randomized double-blind multicenter placebo-controlled trial; 84 patients aged 6–65 with pathogenic PANK2 variants
    exposure
    24 weeks; fosmetpantotenate 41 versus placebo 43. Adults and children at least 40 kg: 300 mg three times/day; children 20–<40 kg: 150 mg three times/day; children <20 kg: 75 mg three times/day.
    limitations
    Genetic disease, not nutritional B5 deficiency. No measure of brain target engagement was available, so a negative functional endpoint does not locate the failed biochemical step. Sponsor-funded trial; no general safety or dietary-efficacy conclusion.
    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 prodrug did not improve the trial’s primary daily-function outcome.
    primary_references
    [b5-clin-fort2021] Fosmetpantotenate Randomized Controlled Trial in Pantothenate Kinase-Associated Neurodegeneration. (2021). https://pubmed.ncbi.nlm.nih.gov/33200489/ DOI: 10.1002/mds.28392
    tissue_or_cell_type
    Patient/surrogate functional rating and clinician-rated motor performance
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1439–1451

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · FORT randomized double-blind multicenter placebo-controlled trial; 84 patients aged 6–65 with pathogenic PANK2 variants · source_derived_draft · unverified_draft

    ### b5-clin-fort-adl-null FORT found no significant difference in 24-week PKAN-ADL change between fosmetpantotenate and placebo: adjusted difference −0.09 points, 95% CI −1.69 to 1.51, P=0.9115. 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 prodrug did not improve the trial’s primary daily-function outcome. organism: Homo sapiens tissue_or_cell_type: Patient/surrogate functional rating and clinician-rated motor performance experimental_model: FORT randomized double-blind multicenter placebo-controlled trial; 84 patients aged 6–65 with pathogenic PANK2 variants limitations: Genetic disease, not nutritional B5 deficiency. No measure of brain target engagement was available, so a negative functional endpoint does not locate the failed biochemical step. Sponsor-funded trial; no general safety or dietary-efficacy conclusion. exposure: 24 weeks; fosmetpantotenate 41 versus placebo 43. Adults and children at least 40 kg: 300 mg three times/day; children 20–<40 kg: 150 mg three times/day; children <20 kg: 75 mg three times/day. cross_nutrient: false evidence_location: Full primary BioC Methods, Results and Discussion. [b5-clin-fort2021] Fosmetpantotenate Randomized Controlled Trial in Pantothenate Kinase-Associated Neurodegeneration. (2021). https://pubmed.ncbi.nlm.nih.gov/33200489/ DOI: 10.1002/mds.28392
    Complete structured claim and evidence

  3. The secondary UPDRS III motor endpoint also showed no significant treatment difference; mean 24-week changes were +0.7 points with fosmetpantotenate and −1.0 with placebo.

    Fosmetpantotenate → PKAN UPDRS III motor score source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    evidence_location
    Full primary BioC Methods, Results and Discussion.
    experimental_model
    FORT randomized double-blind multicenter placebo-controlled trial; 84 patients aged 6–65 with pathogenic PANK2 variants
    exposure
    24 weeks; fosmetpantotenate 41 versus placebo 43. Adults and children at least 40 kg: 300 mg three times/day; children 20–<40 kg: 150 mg three times/day; children <20 kg: 75 mg three times/day.
    limitations
    Genetic disease, not nutritional B5 deficiency. No measure of brain target engagement was available, so a negative functional endpoint does not locate the failed biochemical step. Sponsor-funded trial; no general safety or dietary-efficacy conclusion.
    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 clinician-rated motor outcome also failed to show benefit.
    primary_references
    [b5-clin-fort2021] Fosmetpantotenate Randomized Controlled Trial in Pantothenate Kinase-Associated Neurodegeneration. (2021). https://pubmed.ncbi.nlm.nih.gov/33200489/ DOI: 10.1002/mds.28392
    tissue_or_cell_type
    Patient/surrogate functional rating and clinician-rated motor performance
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1453–1465

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · FORT randomized double-blind multicenter placebo-controlled trial; 84 patients aged 6–65 with pathogenic PANK2 variants · source_derived_draft · unverified_draft

    ### b5-clin-fort-motor-null The secondary UPDRS III motor endpoint also showed no significant treatment difference; mean 24-week changes were +0.7 points with fosmetpantotenate and −1.0 with placebo. 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 clinician-rated motor outcome also failed to show benefit. organism: Homo sapiens tissue_or_cell_type: Patient/surrogate functional rating and clinician-rated motor performance experimental_model: FORT randomized double-blind multicenter placebo-controlled trial; 84 patients aged 6–65 with pathogenic PANK2 variants limitations: Genetic disease, not nutritional B5 deficiency. No measure of brain target engagement was available, so a negative functional endpoint does not locate the failed biochemical step. Sponsor-funded trial; no general safety or dietary-efficacy conclusion. exposure: 24 weeks; fosmetpantotenate 41 versus placebo 43. Adults and children at least 40 kg: 300 mg three times/day; children 20–<40 kg: 150 mg three times/day; children <20 kg: 75 mg three times/day. cross_nutrient: false evidence_location: Full primary BioC Methods, Results and Discussion. [b5-clin-fort2021] Fosmetpantotenate Randomized Controlled Trial in Pantothenate Kinase-Associated Neurodegeneration. (2021). https://pubmed.ncbi.nlm.nih.gov/33200489/ DOI: 10.1002/mds.28392
    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