Component

Vitamin K

Family of vitamin K compounds that support vitamin K-dependent protein carboxylation; not restricted to menaquinone-7 or K2.

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

What it acts on

  1. Oral vitamin K rescued the lethal bleeding phenotype of Vkorc1-null mice.

    Vitamin K → Hemorrhage source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/k2-research/19492146.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4f3957681861ebb8860b46b4a29e6b9c142ba79e7abff1af925dd48b7f0e0c6c", "start_char": 0, "end_char": 1237, "text_sha256": "4f3957681861ebb8860b46b4a29e6b9c142ba79e7abff1af925dd48b7f0e0c6c"}
    experimental_model
    Knockout and oral vitamin K rescue
    exposure
    Vkorc1 deletion
    limitations
    Shared vitamin K pathway; the rescue is not proof that K2 supplements replace medical management. Later alternative reductase findings prevent treating the paper as evidence that no bypass can exist.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Mice
    plain_language
    Cofactor supply could bypass enough of the defect in this experimental model.
    primary_references
    [k2-p19492146] VKORC1 deficiency in mice causes early postnatal lethality due to severe bleeding. (2009). https://pubmed.ncbi.nlm.nih.gov/19492146/ DOI: 10.1160/th09-03-0204
    tissue_or_cell_type
    Postnatal coagulation and skeletal development
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 916–927

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Knockout and oral vitamin K rescue · source_derived_draft · unverified_draft

    ### k2-vkor-rescue Oral vitamin K rescued the lethal bleeding phenotype of Vkorc1-null mice. Condition category: machinery_impairment nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Cofactor supply could bypass enough of the defect in this experimental model. organism: Mice tissue_or_cell_type: Postnatal coagulation and skeletal development experimental_model: Knockout and oral vitamin K rescue limitations: Shared vitamin K pathway; the rescue is not proof that K2 supplements replace medical management. Later alternative reductase findings prevent treating the paper as evidence that no bypass can exist. exposure: Vkorc1 deletion evidence_span: {"source_cache": "artifacts/k2-research/19492146.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4f3957681861ebb8860b46b4a29e6b9c142ba79e7abff1af925dd48b7f0e0c6c", "start_char": 0, "end_char": 1237, "text_sha256": "4f3957681861ebb8860b46b4a29e6b9c142ba79e7abff1af925dd48b7f0e0c6c"} [k2-p19492146] VKORC1 deficiency in mice causes early postnatal lethality due to severe bleeding. (2009). https://pubmed.ncbi.nlm.nih.gov/19492146/ DOI: 10.1160/th09-03-0204
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. A concentrated vitamin K-dependent carboxylase preparation converted glutamate residues of decarboxylated bovine osteocalcin into gamma-carboxyglutamate in vitro.

    Gamma-glutamyl carboxylase / GGCX → Decarboxylated osteocalcin source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Vitamin D regulates osteocalcin expression in specified models; vitamin K-dependent carboxylation modifies its protein product through a distinct enzyme reaction.
    evidence_locator
    Abstract: reported experimental results
    evidence_scope
    D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison.
    experimental_model
    Microsomal vitamin K-dependent carboxylase enriched about 100-fold; bovine osteocalcin substrate and CO2-incorporation assay
    exposure
    50 mM bicarbonate, excess enriched carboxylase and limiting decarboxylated osteocalcin; vitamin K-dependent reaction conditions.
    limitations
    In-vitro modification of a defined substrate; no D-plus-K supplementation regimen, K2-specific necessity, improved fracture outcome or obligatory supplement pairing was tested.
    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
    Bos taurus osteocalcin; liver-derived enzyme preparation
    plain_language
    Osteocalcin needs a separate vitamin K-dependent protein-modification step; making more osteocalcin is not the same reaction.
    primary_references
    [vdm-soute1987] Vitamin K-dependent carboxylase: increased efficiency of the carboxylation reaction. (1987). https://pubmed.ncbi.nlm.nih.gov/3495900/ DOI: 10.1055/s-0038-1651066
    tissue_or_cell_type
    Cell-free enzyme assay

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 889–903

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Microsomal vitamin K-dependent carboxylase enriched about 100-fold; bovine osteocalcin substrate and CO2-incorporation assay · source_derived_draft · unverified_draft

    ### vdm-vitamin-k-carboxylase-modifies-osteocalcin A concentrated vitamin K-dependent carboxylase preparation converted glutamate residues of decarboxylated bovine osteocalcin into gamma-carboxyglutamate in vitro. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Osteocalcin needs a separate vitamin K-dependent protein-modification step; making more osteocalcin is not the same reaction. organism: Bos taurus osteocalcin; liver-derived enzyme preparation tissue_or_cell_type: Cell-free enzyme assay experimental_model: Microsomal vitamin K-dependent carboxylase enriched about 100-fold; bovine osteocalcin substrate and CO2-incorporation assay limitations: In-vitro modification of a defined substrate; no D-plus-K supplementation regimen, K2-specific necessity, improved fracture outcome or obligatory supplement pairing was tested. exposure: 50 mM bicarbonate, excess enriched carboxylase and limiting decarboxylated osteocalcin; vitamin K-dependent reaction conditions. cross_nutrient: Vitamin D regulates osteocalcin expression in specified models; vitamin K-dependent carboxylation modifies its protein product through a distinct enzyme reaction. 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-soute1987] Vitamin K-dependent carboxylase: increased efficiency of the carboxylation reaction. (1987). https://pubmed.ncbi.nlm.nih.gov/3495900/ DOI: 10.1055/s-0038-1651066
    Complete structured claim and evidence

  2. Plasma phylloquinone and percentage undercarboxylated osteocalcin did not change significantly with vitamin E supplementation despite increased PIVKA-II.

    RRR-alpha-tocopherol → Undercarboxylated osteocalcin source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    true
    experimental_model
    Two independent 12-week randomized trials; 38 adults with rheumatoid arthritis and 32 healthy men
    exposure
    RRR-alpha-tocopherol 1000 IU/day; participants were not receiving oral anticoagulant therapy.
    limitations
    Biochemical marker study, not a bleeding-events trial. The study does not identify CYP4F2 activation, direct GGCX inhibition or clinical vitamin K deficiency as the causal route.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Homo sapiens
    plain_language
    The vitamin K-related markers did not all respond in the same way.
    primary_references
    [e-clin-booth2004] Effect of vitamin E supplementation on vitamin K status in adults with normal coagulation status. (2004). https://pubmed.ncbi.nlm.nih.gov/15213041/ DOI: 10.1093/ajcn/80.1.143
    tissue_or_cell_type
    Circulation and vitamin K-dependent carboxylation

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1271–1282

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Two independent 12-week randomized trials; 38 adults with rheumatoid arthritis and 32 healthy men · source_derived_draft · unverified_draft

    ### e-clin-vitamin-k-marker-boundary Plasma phylloquinone and percentage undercarboxylated osteocalcin did not change significantly with vitamin E supplementation despite increased PIVKA-II. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: The vitamin K-related markers did not all respond in the same way. organism: Homo sapiens tissue_or_cell_type: Circulation and vitamin K-dependent carboxylation experimental_model: Two independent 12-week randomized trials; 38 adults with rheumatoid arthritis and 32 healthy men limitations: Biochemical marker study, not a bleeding-events trial. The study does not identify CYP4F2 activation, direct GGCX inhibition or clinical vitamin K deficiency as the causal route. exposure: RRR-alpha-tocopherol 1000 IU/day; participants were not receiving oral anticoagulant therapy. cross_nutrient: true [e-clin-booth2004] Effect of vitamin E supplementation on vitamin K status in adults with normal coagulation status. (2004). https://pubmed.ncbi.nlm.nih.gov/15213041/ DOI: 10.1093/ajcn/80.1.143
    Complete structured claim and evidence

  3. High-dose RRR-alpha-tocopherol increased PIVKA-II in both 12-week adult trials: mean values rose from 1.7 to 11.9 ng/mL and from 1.8 to 5.3 ng/mL.

    RRR-alpha-tocopherol → Undercarboxylated prothrombin / PIVKA-II source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    true
    experimental_model
    Two independent 12-week randomized trials; 38 adults with rheumatoid arthritis and 32 healthy men
    exposure
    RRR-alpha-tocopherol 1000 IU/day; participants were not receiving oral anticoagulant therapy.
    limitations
    Biochemical marker study, not a bleeding-events trial. The study does not identify CYP4F2 activation, direct GGCX inhibition or clinical vitamin K deficiency as the causal route.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Homo sapiens
    plain_language
    High-dose vitamin E altered a vitamin K-dependent clotting-protein marker.
    primary_references
    [e-clin-booth2004] Effect of vitamin E supplementation on vitamin K status in adults with normal coagulation status. (2004). https://pubmed.ncbi.nlm.nih.gov/15213041/ DOI: 10.1093/ajcn/80.1.143
    tissue_or_cell_type
    Circulation and vitamin K-dependent carboxylation

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1258–1269

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Two independent 12-week randomized trials; 38 adults with rheumatoid arthritis and 32 healthy men · source_derived_draft · unverified_draft

    ### e-clin-vitamin-k-pivka High-dose RRR-alpha-tocopherol increased PIVKA-II in both 12-week adult trials: mean values rose from 1.7 to 11.9 ng/mL and from 1.8 to 5.3 ng/mL. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: High-dose vitamin E altered a vitamin K-dependent clotting-protein marker. organism: Homo sapiens tissue_or_cell_type: Circulation and vitamin K-dependent carboxylation experimental_model: Two independent 12-week randomized trials; 38 adults with rheumatoid arthritis and 32 healthy men limitations: Biochemical marker study, not a bleeding-events trial. The study does not identify CYP4F2 activation, direct GGCX inhibition or clinical vitamin K deficiency as the causal route. exposure: RRR-alpha-tocopherol 1000 IU/day; participants were not receiving oral anticoagulant therapy. cross_nutrient: true [e-clin-booth2004] Effect of vitamin E supplementation on vitamin K status in adults with normal coagulation status. (2004). https://pubmed.ncbi.nlm.nih.gov/15213041/ DOI: 10.1093/ajcn/80.1.143
    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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