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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What it acts on
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 evidenceActive 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 evidencePhospho1-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
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)
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 evidenceHuman 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
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.