Component

Phosphoethanolamine/phosphocholine phosphatase PHOSPHO1

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

6 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

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. Combined loss of PHOSPHO1 and ALPL prevented skeletal mineralization in the reported double-null mouse embryos.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    experimental_model
    Phospho1/Alpl double-null embryos
    limitations
    Severe genetic disruption is not equivalent to low dietary calcium; isolated exceptions and developmental timing matter.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Mus musculus
    plain_language
    These phosphate-handling enzymes provide complementary support for mineral formation.
    primary_references
    [yadav2011] Loss of skeletal mineralization by the simultaneous ablation of PHOSPHO1 and alkaline phosphatase function: a unified model of the mechanisms of initiation of skeletal calcification (2011). https://pubmed.ncbi.nlm.nih.gov/20684022/ DOI: 10.1002/jbmr.195
    tissue_or_cell_type
    Developing skeleton
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Calcium: mechanism-first literature curation (2026-09-17) · lines 954–963

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Phospho1/Alpl double-null embryos · source_derived_draft · unverified_draft

    ### phospho1-alpl-double-loss-mineralization Combined loss of PHOSPHO1 and ALPL prevented skeletal mineralization in the reported double-null mouse embryos. Condition category: machinery_impairment nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: These phosphate-handling enzymes provide complementary support for mineral formation. organism: Mus musculus tissue_or_cell_type: Developing skeleton experimental_model: Phospho1/Alpl double-null embryos limitations: Severe genetic disruption is not equivalent to low dietary calcium; isolated exceptions and developmental timing matter. [yadav2011] Loss of skeletal mineralization by the simultaneous ablation of PHOSPHO1 and alkaline phosphatase function: a unified model of the mechanisms of initiation of skeletal calcification (2011). https://pubmed.ncbi.nlm.nih.gov/20684022/ DOI: 10.1002/jbmr.195
    Complete structured claim and evidence
  2. Active PHOSPHO1 was detected inside osteoblast-derived matrix vesicles; phosphoethanolamine hydrolase activity became accessible after vesicle sonication.

    Experimental context and source evidence
    compartment_description
    Matrix-vesicle lumen
    experimental_model
    Localization and activity assays, including Alpl-deficient vesicles
    limitations
    Localization does not establish the sole route for vesicle phosphate or calcium entry.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Mus musculus
    plain_language
    Mineralizing vesicles contain phosphate-generating machinery within their membrane.
    primary_references
    [roberts2007] Functional involvement of PHOSPHO1 in matrix vesicle-mediated skeletal mineralization (2007). https://pubmed.ncbi.nlm.nih.gov/17227223/ DOI: 10.1359/jbmr.070108
    tissue_or_cell_type
    Osteoblast-derived matrix vesicles

    Calcium: mechanism-first literature curation (2026-09-17) · lines 919–929

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Localization and activity assays, including Alpl-deficient vesicles · source_derived_draft · unverified_draft

    ### phospho1-in-matrix-vesicles Active PHOSPHO1 was detected inside osteoblast-derived matrix vesicles; phosphoethanolamine hydrolase activity became accessible after vesicle sonication. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Mineralizing vesicles contain phosphate-generating machinery within their membrane. organism: Mus musculus tissue_or_cell_type: Osteoblast-derived matrix vesicles experimental_model: Localization and activity assays, including Alpl-deficient vesicles limitations: Localization does not establish the sole route for vesicle phosphate or calcium entry. compartment_description: Matrix-vesicle lumen [roberts2007] Functional involvement of PHOSPHO1 in matrix vesicle-mediated skeletal mineralization (2007). https://pubmed.ncbi.nlm.nih.gov/17227223/ DOI: 10.1359/jbmr.070108
    Complete structured claim and evidence
  3. Phospho1-null mouse incisors were hypomineralized, with a further defect after loss of one Alpl allele.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    experimental_model
    Phospho1-null and Phospho1-null/Alpl-heterozygous mice
    limitations
    A developmental machinery defect; it does not establish dietary calcium deficiency as its cause.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Mus musculus
    plain_language
    Tooth dentin depends on mineral-processing enzymes as well as mineral supply.
    primary_references
    [mckee2013] Compounded PHOSPHO1/ALPL deficiencies reduce dentin mineralization (2013). https://pmc.ncbi.nlm.nih.gov/articles/PMC3711567/ DOI: 10.1177/0022034513490958
    tissue_or_cell_type
    Incisor dentin and odontoblast-associated vesicles
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Calcium: mechanism-first literature curation (2026-09-17) · lines 965–974

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Phospho1-null and Phospho1-null/Alpl-heterozygous mice · source_derived_draft · unverified_draft

    ### phospho1-loss-reduces-dentin-mineralization Phospho1-null mouse incisors were hypomineralized, with a further defect after loss of one Alpl allele. Condition category: machinery_impairment nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Tooth dentin depends on mineral-processing enzymes as well as mineral supply. organism: Mus musculus tissue_or_cell_type: Incisor dentin and odontoblast-associated vesicles experimental_model: Phospho1-null and Phospho1-null/Alpl-heterozygous mice limitations: A developmental machinery defect; it does not establish dietary calcium deficiency as its cause. [mckee2013] Compounded PHOSPHO1/ALPL deficiencies reduce dentin mineralization (2013). https://pmc.ncbi.nlm.nih.gov/articles/PMC3711567/ DOI: 10.1177/0022034513490958
    Complete structured claim and evidence

What acts on it

  1. Recombinant human PHOSPHO1 showed strong Mg dependence when hydrolyzing phosphoethanolamine and phosphocholine.

    Experimental context and source evidence
    cross_nutrient
    Magnesium -> PHOSPHO1 -> phosphate production; joins the existing calcium PHOSPHO1 records.
    experimental_model
    Purified recombinant phosphatase assays.
    limitations
    Enzyme evidence does not measure the effect of oral Mg on bone; substrate Km values are not Mg deficiency thresholds.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Homo sapiens
    plain_language
    Magnesium helps a phosphate-releasing enzyme already connected to calcium mineralization.
    primary_references
    [mg-roberts2004] Human PHOSPHO1 exhibits high specific phosphoethanolamine and phosphocholine phosphatase activities (2004). https://pubmed.ncbi.nlm.nih.gov/15175005/ DOI: 10.1042/bj20040511
    tissue_or_cell_type
    Purified recombinant human PHOSPHO1

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1455–1465

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified recombinant phosphatase assays. · source_derived_draft · unverified_draft

    ### mg-phospho1-cofactor Recombinant human PHOSPHO1 showed strong Mg dependence when hydrolyzing phosphoethanolamine and phosphocholine. Condition category: normal nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Magnesium helps a phosphate-releasing enzyme already connected to calcium mineralization. organism: Homo sapiens tissue_or_cell_type: Purified recombinant human PHOSPHO1 experimental_model: Purified recombinant phosphatase assays. limitations: Enzyme evidence does not measure the effect of oral Mg on bone; substrate Km values are not Mg deficiency thresholds. cross_nutrient: Magnesium -> PHOSPHO1 -> phosphate production; joins the existing calcium PHOSPHO1 records. [mg-roberts2004] Human PHOSPHO1 exhibits high specific phosphoethanolamine and phosphocholine phosphatase activities (2004). https://pubmed.ncbi.nlm.nih.gov/15175005/ DOI: 10.1042/bj20040511
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Human PHOSPHO1 also hydrolyzes phosphocholine, producing inorganic phosphate and choline.

    Experimental context and source evidence
    experimental_model
    Purified-enzyme substrate assay
    limitations
    This reaction uses magnesium-dependent machinery; calcium is the eventual mineral constituent, not the demonstrated phosphatase cofactor.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Homo sapiens
    plain_language
    A second phospholipid-headgroup metabolite can supply phosphate.
    primary_references
    [roberts2004] Human PHOSPHO1 exhibits high specific phosphoethanolamine and phosphocholine phosphatase activities (2004). https://pubmed.ncbi.nlm.nih.gov/15175005/ DOI: 10.1042/BJ20040511
    tissue_or_cell_type
    Recombinant enzyme

    Calcium: mechanism-first literature curation (2026-09-17) · lines 908–917

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified-enzyme substrate assay · source_derived_draft · unverified_draft

    ### phospho1-phosphocholine-hydrolysis Human PHOSPHO1 also hydrolyzes phosphocholine, producing inorganic phosphate and choline. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A second phospholipid-headgroup metabolite can supply phosphate. organism: Homo sapiens tissue_or_cell_type: Recombinant enzyme experimental_model: Purified-enzyme substrate assay limitations: This reaction uses magnesium-dependent machinery; calcium is the eventual mineral constituent, not the demonstrated phosphatase cofactor. [roberts2004] Human PHOSPHO1 exhibits high specific phosphoethanolamine and phosphocholine phosphatase activities (2004). https://pubmed.ncbi.nlm.nih.gov/15175005/ DOI: 10.1042/BJ20040511
    Complete structured claim and evidence
  2. Human PHOSPHO1 hydrolyzes phosphoethanolamine, releasing inorganic phosphate and ethanolamine; the enzyme requires Mg2+ in the assay.

    Experimental context and source evidence
    experimental_model
    Purified-enzyme substrate assay
    limitations
    Catalytic capacity does not quantify phosphate supply in vivo; Pi denotes pH-dependent protonation states.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Homo sapiens
    plain_language
    PHOSPHO1 can release phosphate from a membrane-headgroup metabolite.
    primary_references
    [roberts2004] Human PHOSPHO1 exhibits high specific phosphoethanolamine and phosphocholine phosphatase activities (2004). https://pubmed.ncbi.nlm.nih.gov/15175005/ DOI: 10.1042/BJ20040511
    tissue_or_cell_type
    Recombinant enzyme; mineralizing-cell context

    Calcium: mechanism-first literature curation (2026-09-17) · lines 897–906

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified-enzyme substrate assay · source_derived_draft · unverified_draft

    ### phospho1-phosphoethanolamine-hydrolysis Human PHOSPHO1 hydrolyzes phosphoethanolamine, releasing inorganic phosphate and ethanolamine; the enzyme requires Mg2+ in the assay. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: PHOSPHO1 can release phosphate from a membrane-headgroup metabolite. organism: Homo sapiens tissue_or_cell_type: Recombinant enzyme; mineralizing-cell context experimental_model: Purified-enzyme substrate assay limitations: Catalytic capacity does not quantify phosphate supply in vivo; Pi denotes pH-dependent protonation states. [roberts2004] Human PHOSPHO1 exhibits high specific phosphoethanolamine and phosphocholine phosphatase activities (2004). https://pubmed.ncbi.nlm.nih.gov/15175005/ DOI: 10.1042/BJ20040511
    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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