Component

Osteocalcin / BGLAP

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

8 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. Vitamin K-dependent protein propeptide binding stabilized GGCX transmembrane helices 6 and 7 and created its vitamin-K-binding pocket.

    Osteocalcin / BGLAP → Gamma-glutamyl carboxylase / GGCX source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/k2-research/39880952.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "eb8e6d00eecd7c5c780921cae3f804fab60e919301eeb16e9909f36293aaa653", "start_char": 0, "end_char": 1230, "text_sha256": "eb8e6d00eecd7c5c780921cae3f804fab60e919301eeb16e9909f36293aaa653"}
    experimental_model
    Cryo-EM, binding, cell assays and molecular dynamics
    exposure
    Apo, osteocalcin-bound and vitamin-K-bound structures
    limitations
    Shared vitamin K chemistry; the abstract does not establish K2 exclusivity or identical kinetics for every menaquinone.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Human GGCX
    plain_language
    The target protein helps organize the enzyme that modifies it.
    primary_references
    [k2-p39880952] Structure and mechanism of vitamin-K-dependent γ-glutamyl carboxylase. (2025). https://pubmed.ncbi.nlm.nih.gov/39880952/ DOI: 10.1038/s41586-024-08484-9
    tissue_or_cell_type
    Endoplasmic-reticulum membrane enzyme

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 383–394

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cryo-EM, binding, cell assays and molecular dynamics · source_derived_draft · unverified_draft

    ### k2-ggcx-osteocalcin-binding Vitamin K-dependent protein propeptide binding stabilized GGCX transmembrane helices 6 and 7 and created its vitamin-K-binding pocket. Condition category: normal nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The target protein helps organize the enzyme that modifies it. organism: Human GGCX tissue_or_cell_type: Endoplasmic-reticulum membrane enzyme experimental_model: Cryo-EM, binding, cell assays and molecular dynamics limitations: Shared vitamin K chemistry; the abstract does not establish K2 exclusivity or identical kinetics for every menaquinone. exposure: Apo, osteocalcin-bound and vitamin-K-bound structures evidence_span: {"source_cache": "artifacts/k2-research/39880952.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "eb8e6d00eecd7c5c780921cae3f804fab60e919301eeb16e9909f36293aaa653", "start_char": 0, "end_char": 1230, "text_sha256": "eb8e6d00eecd7c5c780921cae3f804fab60e919301eeb16e9909f36293aaa653"} [k2-p39880952] Structure and mechanism of vitamin-K-dependent γ-glutamyl carboxylase. (2025). https://pubmed.ncbi.nlm.nih.gov/39880952/ DOI: 10.1038/s41586-024-08484-9
    Complete structured claim and evidence

What acts on it

  1. In primary calvarial osteoblast cultures from the same transgenic mice, calcitriol inhibited endogenous mouse osteocalcin accumulation while increasing human osteocalcin production.

    Calcitriol → Osteocalcin / BGLAP source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Vitamin D–vitamin K boundary: gene expression and carboxylation are distinct, and osteocalcin transcription is species-dependent.
    evidence_locator
    Abstract: reported experimental results
    evidence_scope
    D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison.
    experimental_model
    Primary calvarial osteoblasts from human-osteocalcin-transgenic mice; species-specific protein assays
    exposure
    Calcitriol exposure of primary cultures; exact culture dose/time not given in the retrieved abstract.
    limitations
    Species and gene-regulatory context explain the difference; this is not an orange scientific conflict and does not predict human fracture outcomes.
    nutrient
    Vitamin D2 and D3 · Vitamin D2 and D3
    nutrient_topic
    Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
    organism
    Mus musculus with human BGLAP transgene
    plain_language
    Mouse and human osteocalcin genes responded differently in the same experimental setting.
    primary_references
    [vdm-zhang1997] Analysis of osteocalcin expression in transgenic mice reveals a species difference in vitamin D regulation of mouse and human osteocalcin genes. (1997). https://pubmed.ncbi.nlm.nih.gov/9333117/ DOI: 10.1359/jbmr.1997.12.10.1570
    tissue_or_cell_type
    Calvarial osteoblast culture

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 873–887

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary calvarial osteoblasts from human-osteocalcin-transgenic mice; species-specific protein assays · source_derived_draft · unverified_draft

    ### vdm-calcitriol-mouse-osteocalcin-culture-scope In primary calvarial osteoblast cultures from the same transgenic mice, calcitriol inhibited endogenous mouse osteocalcin accumulation while increasing human osteocalcin production. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Mouse and human osteocalcin genes responded differently in the same experimental setting. organism: Mus musculus with human BGLAP transgene tissue_or_cell_type: Calvarial osteoblast culture experimental_model: Primary calvarial osteoblasts from human-osteocalcin-transgenic mice; species-specific protein assays limitations: Species and gene-regulatory context explain the difference; this is not an orange scientific conflict and does not predict human fracture outcomes. exposure: Calcitriol exposure of primary cultures; exact culture dose/time not given in the retrieved abstract. cross_nutrient: Vitamin D–vitamin K boundary: gene expression and carboxylation are distinct, and osteocalcin transcription is species-dependent. evidence_locator: Abstract: reported experimental results nutrient: Vitamin D2 and D3 evidence_scope: D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison. [vdm-zhang1997] Analysis of osteocalcin expression in transgenic mice reveals a species difference in vitamin D regulation of mouse and human osteocalcin genes. (1997). https://pubmed.ncbi.nlm.nih.gov/9333117/ DOI: 10.1359/jbmr.1997.12.10.1570
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Calcitriol increased human osteocalcin mRNA about 1.8-fold in calvaria of mice carrying the human osteocalcin genomic transgene.

    Calcitriol → Human BGLAP mRNA source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Vitamin D–vitamin K boundary: vitamin D-regulated osteocalcin expression is distinct from subsequent vitamin K-dependent carboxylation.
    evidence_locator
    Abstract: reported experimental results
    evidence_scope
    D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison.
    experimental_model
    Human osteocalcin genomic transgene in mice; calvarial mRNA analysis
    exposure
    Repeated calcitriol administration; exact dose and calvarial mRNA collection time not specified in the retrieved abstract.
    limitations
    Human transgene in mouse tissue is not a human supplementation trial. Transcript induction does not measure vitamin K-dependent carboxylation.
    nutrient
    Vitamin D2 and D3 · Vitamin D2 and D3
    nutrient_topic
    Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
    organism
    Mus musculus with human BGLAP transgene
    plain_language
    The human osteocalcin gene responded to active vitamin D in this engineered mouse model.
    primary_references
    [vdm-zhang1997] Analysis of osteocalcin expression in transgenic mice reveals a species difference in vitamin D regulation of mouse and human osteocalcin genes. (1997). https://pubmed.ncbi.nlm.nih.gov/9333117/ DOI: 10.1359/jbmr.1997.12.10.1570
    tissue_or_cell_type
    Calvaria

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 857–871

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human osteocalcin genomic transgene in mice; calvarial mRNA analysis · source_derived_draft · unverified_draft

    ### vdm-calcitriol-induces-human-osteocalcin-transgene Calcitriol increased human osteocalcin mRNA about 1.8-fold in calvaria of mice carrying the human osteocalcin genomic transgene. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The human osteocalcin gene responded to active vitamin D in this engineered mouse model. organism: Mus musculus with human BGLAP transgene tissue_or_cell_type: Calvaria experimental_model: Human osteocalcin genomic transgene in mice; calvarial mRNA analysis limitations: Human transgene in mouse tissue is not a human supplementation trial. Transcript induction does not measure vitamin K-dependent carboxylation. exposure: Repeated calcitriol administration; exact dose and calvarial mRNA collection time not specified in the retrieved abstract. cross_nutrient: Vitamin D–vitamin K boundary: vitamin D-regulated osteocalcin expression is distinct from subsequent vitamin K-dependent carboxylation. evidence_locator: Abstract: reported experimental results nutrient: Vitamin D2 and D3 evidence_scope: D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison. [vdm-zhang1997] Analysis of osteocalcin expression in transgenic mice reveals a species difference in vitamin D regulation of mouse and human osteocalcin genes. (1997). https://pubmed.ncbi.nlm.nih.gov/9333117/ DOI: 10.1359/jbmr.1997.12.10.1570
    Complete structured claim and evidence

  2. Orthosilicic acid increased phosphorylated SMAD1/5 and RUNX2 expression alongside osteogenic markers.

    Orthosilicic acid / Si(OH)4 → Human SMAD1/SMAD5 signaling proteins source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human osteoblast-like cell lines, 10 micromolar exposure.
    limitations
    Marker regulation does not prove each edge by direct binding.
    nutrient_topic
    Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
    plain_language
    The response extended to downstream bone-development regulators.
    primary_references
    Biological Silicon Stimulates Collagen Type 1 and Osteocalcin Synthesis in Human Osteoblast-Like Cells Through the BMP-2/Smad/RUNX2 Signaling Pathway. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27025722/ · DOI 10.1007/s12011-016-0686-3

    Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 152–158

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human osteoblast-like cell lines, 10 micromolar exposure. · source_derived_draft · unverified_draft

    ## silica-smad-runx2 The response extended to downstream bone-development regulators. Orthosilicic acid increased phosphorylated SMAD1/5 and RUNX2 expression alongside osteogenic markers. Model: Human osteoblast-like cell lines, 10 micromolar exposure. Limitations: Marker regulation does not prove each edge by direct binding. Evidence access: Primary abstract Biological Silicon Stimulates Collagen Type 1 and Osteocalcin Synthesis in Human Osteoblast-Like Cells Through the BMP-2/Smad/RUNX2 Signaling Pathway. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27025722/ · DOI 10.1007/s12011-016-0686-3
    Complete structured claim and evidence

  3. Dietary K1 restriction reduced prothrombin and osteocalcin gamma-carboxylation and lowered plasma K1 and urinary Gla excretion.

    Phylloquinone → Vitamin K-dependent protein gamma-carboxylation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/k2-research/12888638.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c57beda0b2c7bdc471fd6f4bfa926e9f12846f040c95689648f599d6cceae874", "start_char": 0, "end_char": 1461, "text_sha256": "c57beda0b2c7bdc471fd6f4bfa926e9f12846f040c95689648f599d6cceae874"}
    experimental_model
    Metabolic-unit dietary depletion/repletion
    exposure
    K1 restricted to 18 micrograms/day for 28 days, then stepped repletion
    limitations
    The measured endpoint is carboxylation, not an observed clinical clotting failure; restricted-K1 exposure does not define isolated K2 deficiency.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    21 women aged 60–80 years
    plain_language
    A shortfall can appear in protein-modification markers before it is described as a clinical syndrome.
    primary_references
    [k2-p12888638] Dietary phylloquinone depletion and repletion in older women. (2003). https://pubmed.ncbi.nlm.nih.gov/12888638/ DOI: 10.1093/jn/133.8.2565
    tissue_or_cell_type
    Hepatic and extrahepatic protein markers
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 1007–1018

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Metabolic-unit dietary depletion/repletion · source_derived_draft · unverified_draft

    ### k2-dietary-k-prothrombin Dietary K1 restriction reduced prothrombin and osteocalcin gamma-carboxylation and lowered plasma K1 and urinary Gla excretion. Condition category: nutrient_deficiency nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A shortfall can appear in protein-modification markers before it is described as a clinical syndrome. organism: 21 women aged 60–80 years tissue_or_cell_type: Hepatic and extrahepatic protein markers experimental_model: Metabolic-unit dietary depletion/repletion limitations: The measured endpoint is carboxylation, not an observed clinical clotting failure; restricted-K1 exposure does not define isolated K2 deficiency. exposure: K1 restricted to 18 micrograms/day for 28 days, then stepped repletion evidence_span: {"source_cache": "artifacts/k2-research/12888638.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c57beda0b2c7bdc471fd6f4bfa926e9f12846f040c95689648f599d6cceae874", "start_char": 0, "end_char": 1461, "text_sha256": "c57beda0b2c7bdc471fd6f4bfa926e9f12846f040c95689648f599d6cceae874"} [k2-p12888638] Dietary phylloquinone depletion and repletion in older women. (2003). https://pubmed.ncbi.nlm.nih.gov/12888638/ DOI: 10.1093/jn/133.8.2565
    Complete structured claim and evidence

  4. Prothrombin carboxylation normalized at 200 micrograms/day, whereas other vitamin K markers had not all returned to baseline after short repletion up to 450 micrograms/day.

    Phylloquinone → Vitamin K-dependent protein gamma-carboxylation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/k2-research/12888638.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c57beda0b2c7bdc471fd6f4bfa926e9f12846f040c95689648f599d6cceae874", "start_char": 0, "end_char": 1461, "text_sha256": "c57beda0b2c7bdc471fd6f4bfa926e9f12846f040c95689648f599d6cceae874"}
    experimental_model
    Metabolic-unit dietary depletion/repletion
    exposure
    K1 restricted to 18 micrograms/day for 28 days, then stepped repletion
    limitations
    K1 restriction probes shared vitamin K status, not an isolated dietary K2 requirement. Biochemical undercarboxylation is not equivalent to clinical bleeding or fractures.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    21 women aged 60–80 years
    plain_language
    A liver-related marker can recover before an extrahepatic marker.
    primary_references
    [k2-p12888638] Dietary phylloquinone depletion and repletion in older women. (2003). https://pubmed.ncbi.nlm.nih.gov/12888638/ DOI: 10.1093/jn/133.8.2565
    tissue_or_cell_type
    Hepatic and extrahepatic protein markers
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 1020–1031

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Metabolic-unit dietary depletion/repletion · source_derived_draft · unverified_draft

    ### k2-different-repletion Prothrombin carboxylation normalized at 200 micrograms/day, whereas other vitamin K markers had not all returned to baseline after short repletion up to 450 micrograms/day. Condition category: nutrient_deficiency nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A liver-related marker can recover before an extrahepatic marker. organism: 21 women aged 60–80 years tissue_or_cell_type: Hepatic and extrahepatic protein markers experimental_model: Metabolic-unit dietary depletion/repletion limitations: K1 restriction probes shared vitamin K status, not an isolated dietary K2 requirement. Biochemical undercarboxylation is not equivalent to clinical bleeding or fractures. exposure: K1 restricted to 18 micrograms/day for 28 days, then stepped repletion evidence_span: {"source_cache": "artifacts/k2-research/12888638.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c57beda0b2c7bdc471fd6f4bfa926e9f12846f040c95689648f599d6cceae874", "start_char": 0, "end_char": 1461, "text_sha256": "c57beda0b2c7bdc471fd6f4bfa926e9f12846f040c95689648f599d6cceae874"} [k2-p12888638] Dietary phylloquinone depletion and repletion in older women. (2003). https://pubmed.ncbi.nlm.nih.gov/12888638/ DOI: 10.1093/jn/133.8.2565
    Complete structured claim and evidence

  5. MK-7 produced more complete osteocalcin carboxylation than the compared K1 regimen.

    Menaquinone-7 / MK-7 → Gamma-carboxylated osteocalcin source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/k2-research/17158229.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1bf2196600220143fbc5ba85e8aba71b4c8aa931f4a6c47545c3db9570283faf", "start_char": 0, "end_char": 1248, "text_sha256": "1bf2196600220143fbc5ba85e8aba71b4c8aa931f4a6c47545c3db9570283faf"}
    experimental_model
    Comparative human absorption and activity experiments
    exposure
    Phylloquinone versus natto-derived MK-7
    limitations
    Biochemical exposure and activity endpoints, not fracture or cardiovascular-event prevention.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Healthy volunteers
    plain_language
    The biochemical modification changed; clinical bone outcomes were a separate question.
    primary_references
    [k2-p17158229] Vitamin K-containing dietary supplements: comparison of synthetic vitamin K1 and natto-derived menaquinone-7. (2007). https://pubmed.ncbi.nlm.nih.gov/17158229/ DOI: 10.1182/blood-2006-08-040709
    tissue_or_cell_type
    Serum vitamers and osteocalcin

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 305–316

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Comparative human absorption and activity experiments · source_derived_draft · unverified_draft

    ### k2-mk7-oc-carboxylation MK-7 produced more complete osteocalcin carboxylation than the compared K1 regimen. Condition category: normal nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The biochemical modification changed; clinical bone outcomes were a separate question. organism: Healthy volunteers tissue_or_cell_type: Serum vitamers and osteocalcin experimental_model: Comparative human absorption and activity experiments limitations: Biochemical exposure and activity endpoints, not fracture or cardiovascular-event prevention. exposure: Phylloquinone versus natto-derived MK-7 evidence_span: {"source_cache": "artifacts/k2-research/17158229.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1bf2196600220143fbc5ba85e8aba71b4c8aa931f4a6c47545c3db9570283faf", "start_char": 0, "end_char": 1248, "text_sha256": "1bf2196600220143fbc5ba85e8aba71b4c8aa931f4a6c47545c3db9570283faf"} [k2-p17158229] Vitamin K-containing dietary supplements: comparison of synthetic vitamin K1 and natto-derived menaquinone-7. (2007). https://pubmed.ncbi.nlm.nih.gov/17158229/ DOI: 10.1182/blood-2006-08-040709
    Complete structured claim and evidence

  6. RA-treated osteoblasts had reduced alkaline phosphatase and osteocalcin, with lower RUNX2/SP7 protein and PHEX expression.

    All-trans-retinoic acid → Tissue-nonspecific alkaline phosphatase ALPL / TNAP source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Vitamin A -> shared ALPL node already linked to zinc, magnesium and calcium.
    experimental_model
    Same culture experiments.
    limitations
    Parallel marker changes do not prove each mediates the mineralization loss.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Homo sapiens; Mus musculus
    plain_language
    Several components of the bone-building program changed together.
    primary_references
    [va-lind2013] Vitamin a is a negative regulator of osteoblast mineralization (2013). https://pubmed.ncbi.nlm.nih.gov/24340023/ DOI: 10.1371/journal.pone.0082388
    tissue_or_cell_type
    Osteoblasts

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1662–1672

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Same culture experiments. · source_derived_draft · unverified_draft

    ### va-retinoic-acid-osteoblast-markers RA-treated osteoblasts had reduced alkaline phosphatase and osteocalcin, with lower RUNX2/SP7 protein and PHEX expression. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Several components of the bone-building program changed together. organism: Homo sapiens; Mus musculus tissue_or_cell_type: Osteoblasts experimental_model: Same culture experiments. limitations: Parallel marker changes do not prove each mediates the mineralization loss. cross_nutrient: Vitamin A -> shared ALPL node already linked to zinc, magnesium and calcium. [va-lind2013] Vitamin a is a negative regulator of osteoblast mineralization (2013). https://pubmed.ncbi.nlm.nih.gov/24340023/ DOI: 10.1371/journal.pone.0082388
    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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