Component

Progressive ankylosis protein homolog ANKH

Independent biological entity. Read linked claims for experimental scope and context.

5 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. Mouse ANK expression increased saturable radiolabeled PPi uptake into Xenopus oocytes.

    Progressive ankylosis protein homolog ANKH → Inorganic pyrophosphate source_derived_draftungraded
    Experimental context and source evidence
    compartment_description
    Extracellular medium to oocyte
    experimental_model
    Heterologous expression and radiotracer uptake
    limitations
    Influx in this model does not establish physiological PPi efflux; retain alongside later ATP-release results.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Mus musculus protein in Xenopus laevis oocytes
    plain_language
    An earlier assay measured movement into an egg cell, not export from human bone cells.
    primary_references
    [gurley2006] Biochemical and genetic analysis of ANK in arthritis and bone disease (2006). https://pubmed.ncbi.nlm.nih.gov/17186460/ DOI: 10.1086/509881
    tissue_or_cell_type
    Oocyte plasma membrane

    Calcium: mechanism-first literature curation (2026-09-17) · lines 988–998

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Heterologous expression and radiotracer uptake · source_derived_draft · unverified_draft

    ### ank-dependent-ppi-uptake-oocytes Mouse ANK expression increased saturable radiolabeled PPi uptake into Xenopus oocytes. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: An earlier assay measured movement into an egg cell, not export from human bone cells. organism: Mus musculus protein in Xenopus laevis oocytes tissue_or_cell_type: Oocyte plasma membrane experimental_model: Heterologous expression and radiotracer uptake limitations: Influx in this model does not establish physiological PPi efflux; retain alongside later ATP-release results. compartment_description: Extracellular medium to oocyte [gurley2006] Biochemical and genetic analysis of ANK in arthritis and bone disease (2006). https://pubmed.ncbi.nlm.nih.gov/17186460/ DOI: 10.1086/509881
    Complete structured claim and evidence

  2. ANKH expression drove ATP release from HEK293 cells even when ENPP1 was absent.

    Progressive ankylosis protein homolog ANKH → ATP source_derived_draftungraded
    Experimental context and source evidence
    compartment_description
    Cytosol to extracellular medium
    experimental_model
    ANKH expression with ENPP1 deletion controls
    limitations
    Cellular export assay; it does not determine purified ANKH transport stoichiometry in every tissue.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Homo sapiens
    plain_language
    ANKH can provide extracellular ATP for subsequent PPi production.
    primary_references
    [szeri2022] The mineralization regulator ANKH mediates cellular efflux of ATP, not pyrophosphate (2022). https://pmc.ncbi.nlm.nih.gov/articles/PMC9098669/ DOI: 10.1002/jbmr.4528
    tissue_or_cell_type
    HEK293 cells

    Calcium: mechanism-first literature curation (2026-09-17) · lines 1000–1010

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · ANKH expression with ENPP1 deletion controls · source_derived_draft · unverified_draft

    ### ankh-atp-export ANKH expression drove ATP release from HEK293 cells even when ENPP1 was absent. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: ANKH can provide extracellular ATP for subsequent PPi production. organism: Homo sapiens tissue_or_cell_type: HEK293 cells experimental_model: ANKH expression with ENPP1 deletion controls limitations: Cellular export assay; it does not determine purified ANKH transport stoichiometry in every tissue. compartment_description: Cytosol to extracellular medium [szeri2022] The mineralization regulator ANKH mediates cellular efflux of ATP, not pyrophosphate (2022). https://pmc.ncbi.nlm.nih.gov/articles/PMC9098669/ DOI: 10.1002/jbmr.4528
    Complete structured claim and evidence

  3. ANKH-expressing HEK293 cells released citrate; Ank-mutant mice also had depleted bone-matrix citrate.

    Progressive ankylosis protein homolog ANKH → Citrate source_derived_draftungraded
    Experimental context and source evidence
    compartment_description
    Cytosol to extracellular space
    experimental_model
    Metabolomics and Ank-mutant tissue measurements
    limitations
    Citrate is a separate substrate; these findings do not prove that citrate alone explains altered bone strength.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Homo sapiens cells; Mus musculus
    plain_language
    ANKH affects a mineral-associated organic component as well as PPi supply.
    primary_references
    [szeri2020] The membrane protein ANKH is crucial for bone mechanical performance by mediating cellular export of citrate and ATP (2020). https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1008884 DOI: 10.1371/journal.pgen.1008884
    tissue_or_cell_type
    Cell medium and bone matrix

    Calcium: mechanism-first literature curation (2026-09-17) · lines 1024–1034

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Metabolomics and Ank-mutant tissue measurements · source_derived_draft · unverified_draft

    ### ankh-citrate-export ANKH-expressing HEK293 cells released citrate; Ank-mutant mice also had depleted bone-matrix citrate. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: ANKH affects a mineral-associated organic component as well as PPi supply. organism: Homo sapiens cells; Mus musculus tissue_or_cell_type: Cell medium and bone matrix experimental_model: Metabolomics and Ank-mutant tissue measurements limitations: Citrate is a separate substrate; these findings do not prove that citrate alone explains altered bone strength. compartment_description: Cytosol to extracellular space [szeri2020] The membrane protein ANKH is crucial for bone mechanical performance by mediating cellular export of citrate and ATP (2020). https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1008884 DOI: 10.1371/journal.pgen.1008884
    Complete structured claim and evidence

  4. Early ANK-dependent changes in cellular and extracellular PPi motivated a proposal that ANK directly exports PPi.

    Progressive ankylosis protein homolog ANKH → Inorganic pyrophosphate source_derived_draftungraded
    Experimental context and source evidence
    compartment_description
    Plasma membrane
    experimental_model
    Ank genetics and cell PPi measurements
    limitations
    Historical hypothesis, not a current unconditional transport assignment; later ATP/ENPP1 experiments require qualification.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Mus musculus protein; cultured mammalian cells
    plain_language
    An older transport explanation was inferred from changes in PPi distribution.
    primary_references
    [ho2000] Role of the mouse ank gene in control of tissue calcification and arthritis (2000). https://pubmed.ncbi.nlm.nih.gov/10894769/ DOI: 10.1126/science.289.5477.265
    tissue_or_cell_type
    Joint-calcification context

    Calcium: mechanism-first literature curation (2026-09-17) · lines 976–986

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ank genetics and cell PPi measurements · source_derived_draft · unverified_draft

    ### ankh-historical-direct-ppi-export-hypothesis Early ANK-dependent changes in cellular and extracellular PPi motivated a proposal that ANK directly exports PPi. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: An older transport explanation was inferred from changes in PPi distribution. organism: Mus musculus protein; cultured mammalian cells tissue_or_cell_type: Joint-calcification context experimental_model: Ank genetics and cell PPi measurements limitations: Historical hypothesis, not a current unconditional transport assignment; later ATP/ENPP1 experiments require qualification. compartment_description: Plasma membrane [ho2000] Role of the mouse ank gene in control of tissue calcification and arthritis (2000). https://pubmed.ncbi.nlm.nih.gov/10894769/ DOI: 10.1126/science.289.5477.265
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. ENPP1 converts extracellular ATP into AMP and PPi; ANKH-expressing cells lacking ENPP1 released ATP without the accompanying PPi accumulation.

    ATP → Inorganic pyrophosphate source_derived_draftungraded
    Experimental context and source evidence
    compartment_description
    Extracellular space
    experimental_model
    ENPP1-proficient versus deficient cells
    limitations
    Other ectonucleotidases compete for ATP; PPi is not synonymous with orthophosphate.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Homo sapiens
    plain_language
    An extracellular enzyme converts exported ATP into a mineralization inhibitor.
    primary_references
    [szeri2022] The mineralization regulator ANKH mediates cellular efflux of ATP, not pyrophosphate (2022). https://pmc.ncbi.nlm.nih.gov/articles/PMC9098669/ DOI: 10.1002/jbmr.4528
    tissue_or_cell_type
    HEK293 extracellular medium

    Calcium: mechanism-first literature curation (2026-09-17) · lines 1012–1022

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · ENPP1-proficient versus deficient cells · source_derived_draft · unverified_draft

    ### enpp1-atp-to-pyrophosphate ENPP1 converts extracellular ATP into AMP and PPi; ANKH-expressing cells lacking ENPP1 released ATP without the accompanying PPi accumulation. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: An extracellular enzyme converts exported ATP into a mineralization inhibitor. organism: Homo sapiens tissue_or_cell_type: HEK293 extracellular medium experimental_model: ENPP1-proficient versus deficient cells limitations: Other ectonucleotidases compete for ATP; PPi is not synonymous with orthophosphate. compartment_description: Extracellular space [szeri2022] The mineralization regulator ANKH mediates cellular efflux of ATP, not pyrophosphate (2022). https://pmc.ncbi.nlm.nih.gov/articles/PMC9098669/ DOI: 10.1002/jbmr.4528
    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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