Component

RUNX2

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

4 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

Where it participates (unsigned role)

  1. Noggin pretreatment suppressed silicon-associated SMAD1/5 phosphorylation, RUNX2 and collagen expression.

    Noggin-treated human osteoblast-like cultures → Collagen synthesis response to orthosilicic acid source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Human osteoblast-like cell pharmacological experiment.
    limitations
    Noggin is a BMP antagonist, not a uniquely selective proof of BMP2 mediation.
    nutrient_topic
    Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
    plain_language
    Blocking BMP signaling weakened the response.
    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
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 160–166

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

    ## silica-noggin-block Blocking BMP signaling weakened the response. Noggin pretreatment suppressed silicon-associated SMAD1/5 phosphorylation, RUNX2 and collagen expression. Model: Human osteoblast-like cell pharmacological experiment. Limitations: Noggin is a BMP antagonist, not a uniquely selective proof of BMP2 mediation. 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

  2. Orthosilicic acid increased PI3K, phosphorylated Akt and mTOR together with osteogenic markers.

    Orthosilicic acid / Si(OH)4 → Human mechanistic target of rapamycin kinase / MTOR source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human osteoblast-like cell study.
    limitations
    No direct binding target or dietary requirement is established.
    nutrient_topic
    Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
    plain_language
    A growth-related pathway accompanied matrix production.
    primary_references
    Orthosilicic Acid Accelerates Bone Formation in Human Osteoblast-Like Cells Through the PI3K-Akt-mTOR Pathway. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30421162/ · DOI 10.1007/s12011-018-1574-9

    Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 168–174

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

    ## silica-pi3k-mtor A growth-related pathway accompanied matrix production. Orthosilicic acid increased PI3K, phosphorylated Akt and mTOR together with osteogenic markers. Model: Human osteoblast-like cell study. Limitations: No direct binding target or dietary requirement is established. Evidence access: Primary abstract Orthosilicic Acid Accelerates Bone Formation in Human Osteoblast-Like Cells Through the PI3K-Akt-mTOR Pathway. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30421162/ · DOI 10.1007/s12011-018-1574-9
    Complete structured claim and evidence

  3. 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

  4. 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.

    Evidence, AI assistance and curation standards