Component

Vitamin K2 / menaquinone family

Vitamin K2 is a family of menaquinones, including MK-4 and MK-7. These forms participate in the shared vitamin K cycle but differ in synthesis, exposure and studied effects.

6 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 K2 transferred electrons in Drosophila mitochondria and improved ATP production; Heix-mutant defects were rescued by K2.

    Vitamin K2 / menaquinone family → Mitochondrial respiratory electron transfer source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/k2-research/22582012.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1f7c8600fd883b912c1fd697b1bffb6e442e2763230347e5c198d88c0c6bb4cc", "start_char": 0, "end_char": 926, "text_sha256": "1f7c8600fd883b912c1fd697b1bffb6e442e2763230347e5c198d88c0c6bb4cc"}
    experimental_model
    Genetic modifier and mitochondrial function experiments
    exposure
    Heix/Pink1 defects and vitamin K2 rescue
    limitations
    Fly electron-transfer rescue does not establish replacement of human CoQ10 or treatment of Parkinson disease.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Drosophila
    plain_language
    An energy role was found in flies and is recorded with that species boundary.
    primary_references
    [k2-p22582012] Vitamin K2 is a mitochondrial electron carrier that rescues pink1 deficiency. (2012). https://pubmed.ncbi.nlm.nih.gov/22582012/ DOI: 10.1126/science.1218632
    tissue_or_cell_type
    Mitochondria
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 864–875

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

    ### k2-fly-mitochondria Vitamin K2 transferred electrons in Drosophila mitochondria and improved ATP production; Heix-mutant defects were rescued by K2. Condition category: machinery_impairment nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: An energy role was found in flies and is recorded with that species boundary. organism: Drosophila tissue_or_cell_type: Mitochondria experimental_model: Genetic modifier and mitochondrial function experiments limitations: Fly electron-transfer rescue does not establish replacement of human CoQ10 or treatment of Parkinson disease. exposure: Heix/Pink1 defects and vitamin K2 rescue evidence_span: {"source_cache": "artifacts/k2-research/22582012.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1f7c8600fd883b912c1fd697b1bffb6e442e2763230347e5c198d88c0c6bb4cc", "start_char": 0, "end_char": 926, "text_sha256": "1f7c8600fd883b912c1fd697b1bffb6e442e2763230347e5c198d88c0c6bb4cc"} [k2-p22582012] Vitamin K2 is a mitochondrial electron carrier that rescues pink1 deficiency. (2012). https://pubmed.ncbi.nlm.nih.gov/22582012/ DOI: 10.1126/science.1218632
    Complete structured claim and evidence

  2. Vitamin K2 bound and activated human SXR and induced its CYP3A4 target gene in the tested system.

    Vitamin K2 / menaquinone family → Human pregnane X receptor / SXR / PXR / NR1I2 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/k2-research/12920130.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "073faa7585981854cba6f1544fbe593a19b98f2ba6b9aec02c32375171e46617", "start_char": 0, "end_char": 1589, "text_sha256": "073faa7585981854cba6f1544fbe593a19b98f2ba6b9aec02c32375171e46617"}
    experimental_model
    Ligand binding, gene expression and receptor-null mouse cells
    exposure
    Vitamin K2 exposure and receptor deficiency
    limitations
    Preclinical transcription effects; supplement-level target engagement in people is not established. Abstract calls the tested ligand K2 without distinguishing every homologue.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Human osteosarcoma cells and mouse calvarial cells
    plain_language
    K2 can have a receptor-signaling role separate from protein carboxylation.
    primary_references
    [k2-p12920130] Vitamin K2 regulation of bone homeostasis is mediated by the steroid and xenobiotic receptor SXR. (2003). https://pubmed.ncbi.nlm.nih.gov/12920130/ DOI: 10.1074/jbc.m303136200
    tissue_or_cell_type
    SXR/PXR transcription

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 695–706

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ligand binding, gene expression and receptor-null mouse cells · source_derived_draft · unverified_draft

    ### k2-k2-sxr Vitamin K2 bound and activated human SXR and induced its CYP3A4 target gene in the tested system. Condition category: normal nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: K2 can have a receptor-signaling role separate from protein carboxylation. organism: Human osteosarcoma cells and mouse calvarial cells tissue_or_cell_type: SXR/PXR transcription experimental_model: Ligand binding, gene expression and receptor-null mouse cells limitations: Preclinical transcription effects; supplement-level target engagement in people is not established. Abstract calls the tested ligand K2 without distinguishing every homologue. exposure: Vitamin K2 exposure and receptor deficiency evidence_span: {"source_cache": "artifacts/k2-research/12920130.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "073faa7585981854cba6f1544fbe593a19b98f2ba6b9aec02c32375171e46617", "start_char": 0, "end_char": 1589, "text_sha256": "073faa7585981854cba6f1544fbe593a19b98f2ba6b9aec02c32375171e46617"} [k2-p12920130] Vitamin K2 regulation of bone homeostasis is mediated by the steroid and xenobiotic receptor SXR. (2003). https://pubmed.ncbi.nlm.nih.gov/12920130/ DOI: 10.1074/jbc.m303136200
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. CD14 was identified as a primary SXR target responsive to vitamin K2 and rifampicin in osteoblastic cells.

    Human pregnane X receptor / SXR / PXR / NR1I2 → Human CD14 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/k2-research/16606623.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a2c0e756d507fd0cef9dea48e3eedc193084378509ec54bce2c097f8491e4b45", "start_char": 0, "end_char": 1266, "text_sha256": "a2c0e756d507fd0cef9dea48e3eedc193084378509ec54bce2c097f8491e4b45"}
    experimental_model
    Microarray, qPCR and gain/loss-of-function studies
    exposure
    Vitamin K2 and rifampicin/SXR stimulation
    limitations
    Cell transcription and collagen accumulation; not a human fracture study.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Human osteoblastic MG63 cells
    plain_language
    The receptor connects to a separately identifiable downstream gene.
    primary_references
    [k2-p16606623] Steroid and xenobiotic receptor SXR mediates vitamin K2-activated transcription of extracellular matrix-related genes and collagen accumulation in osteoblastic cells. (2006). https://pubmed.ncbi.nlm.nih.gov/16606623/ DOI: 10.1074/jbc.m600896200
    tissue_or_cell_type
    Extracellular-matrix gene regulation

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 747–758

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Microarray, qPCR and gain/loss-of-function studies · source_derived_draft · unverified_draft

    ### k2-sxr-cd14 CD14 was identified as a primary SXR target responsive to vitamin K2 and rifampicin in osteoblastic cells. Condition category: normal nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The receptor connects to a separately identifiable downstream gene. organism: Human osteoblastic MG63 cells tissue_or_cell_type: Extracellular-matrix gene regulation experimental_model: Microarray, qPCR and gain/loss-of-function studies limitations: Cell transcription and collagen accumulation; not a human fracture study. exposure: Vitamin K2 and rifampicin/SXR stimulation evidence_span: {"source_cache": "artifacts/k2-research/16606623.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a2c0e756d507fd0cef9dea48e3eedc193084378509ec54bce2c097f8491e4b45", "start_char": 0, "end_char": 1266, "text_sha256": "a2c0e756d507fd0cef9dea48e3eedc193084378509ec54bce2c097f8491e4b45"} [k2-p16606623] Steroid and xenobiotic receptor SXR mediates vitamin K2-activated transcription of extracellular matrix-related genes and collagen accumulation in osteoblastic cells. (2006). https://pubmed.ncbi.nlm.nih.gov/16606623/ DOI: 10.1074/jbc.m600896200
    Complete structured claim and evidence

  2. MATN2 was identified as a primary SXR target responsive to vitamin K2 and rifampicin in osteoblastic cells.

    Human pregnane X receptor / SXR / PXR / NR1I2 → Human matrilin-2 / MATN2 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/k2-research/16606623.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a2c0e756d507fd0cef9dea48e3eedc193084378509ec54bce2c097f8491e4b45", "start_char": 0, "end_char": 1266, "text_sha256": "a2c0e756d507fd0cef9dea48e3eedc193084378509ec54bce2c097f8491e4b45"}
    experimental_model
    Microarray, qPCR and gain/loss-of-function studies
    exposure
    Vitamin K2 and rifampicin/SXR stimulation
    limitations
    Cell transcription and collagen accumulation; not a human fracture study.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Human osteoblastic MG63 cells
    plain_language
    The receptor connects to a separately identifiable downstream gene.
    primary_references
    [k2-p16606623] Steroid and xenobiotic receptor SXR mediates vitamin K2-activated transcription of extracellular matrix-related genes and collagen accumulation in osteoblastic cells. (2006). https://pubmed.ncbi.nlm.nih.gov/16606623/ DOI: 10.1074/jbc.m600896200
    tissue_or_cell_type
    Extracellular-matrix gene regulation

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 734–745

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Microarray, qPCR and gain/loss-of-function studies · source_derived_draft · unverified_draft

    ### k2-sxr-matn2 MATN2 was identified as a primary SXR target responsive to vitamin K2 and rifampicin in osteoblastic cells. Condition category: normal nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The receptor connects to a separately identifiable downstream gene. organism: Human osteoblastic MG63 cells tissue_or_cell_type: Extracellular-matrix gene regulation experimental_model: Microarray, qPCR and gain/loss-of-function studies limitations: Cell transcription and collagen accumulation; not a human fracture study. exposure: Vitamin K2 and rifampicin/SXR stimulation evidence_span: {"source_cache": "artifacts/k2-research/16606623.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a2c0e756d507fd0cef9dea48e3eedc193084378509ec54bce2c097f8491e4b45", "start_char": 0, "end_char": 1266, "text_sha256": "a2c0e756d507fd0cef9dea48e3eedc193084378509ec54bce2c097f8491e4b45"} [k2-p16606623] Steroid and xenobiotic receptor SXR mediates vitamin K2-activated transcription of extracellular matrix-related genes and collagen accumulation in osteoblastic cells. (2006). https://pubmed.ncbi.nlm.nih.gov/16606623/ DOI: 10.1074/jbc.m600896200
    Complete structured claim and evidence

  3. TSKU was identified as a primary SXR target responsive to vitamin K2 and rifampicin in osteoblastic cells.

    Human pregnane X receptor / SXR / PXR / NR1I2 → Human tsukushi / TSKU source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/k2-research/16606623.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a2c0e756d507fd0cef9dea48e3eedc193084378509ec54bce2c097f8491e4b45", "start_char": 0, "end_char": 1266, "text_sha256": "a2c0e756d507fd0cef9dea48e3eedc193084378509ec54bce2c097f8491e4b45"}
    experimental_model
    Microarray, qPCR and gain/loss-of-function studies
    exposure
    Vitamin K2 and rifampicin/SXR stimulation
    limitations
    Cell transcription and collagen accumulation; not a human fracture study.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Human osteoblastic MG63 cells
    plain_language
    The receptor connects to a separately identifiable downstream gene.
    primary_references
    [k2-p16606623] Steroid and xenobiotic receptor SXR mediates vitamin K2-activated transcription of extracellular matrix-related genes and collagen accumulation in osteoblastic cells. (2006). https://pubmed.ncbi.nlm.nih.gov/16606623/ DOI: 10.1074/jbc.m600896200
    tissue_or_cell_type
    Extracellular-matrix gene regulation

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 721–732

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Microarray, qPCR and gain/loss-of-function studies · source_derived_draft · unverified_draft

    ### k2-sxr-tsku TSKU was identified as a primary SXR target responsive to vitamin K2 and rifampicin in osteoblastic cells. Condition category: normal nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The receptor connects to a separately identifiable downstream gene. organism: Human osteoblastic MG63 cells tissue_or_cell_type: Extracellular-matrix gene regulation experimental_model: Microarray, qPCR and gain/loss-of-function studies limitations: Cell transcription and collagen accumulation; not a human fracture study. exposure: Vitamin K2 and rifampicin/SXR stimulation evidence_span: {"source_cache": "artifacts/k2-research/16606623.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a2c0e756d507fd0cef9dea48e3eedc193084378509ec54bce2c097f8491e4b45", "start_char": 0, "end_char": 1266, "text_sha256": "a2c0e756d507fd0cef9dea48e3eedc193084378509ec54bce2c097f8491e4b45"} [k2-p16606623] Steroid and xenobiotic receptor SXR mediates vitamin K2-activated transcription of extracellular matrix-related genes and collagen accumulation in osteoblastic cells. (2006). https://pubmed.ncbi.nlm.nih.gov/16606623/ DOI: 10.1074/jbc.m600896200
    Complete structured claim and evidence

  4. Human UBIAD1 expression supported conversion of labeled vitamin K precursors to MK-4, identified by deuterium NMR.

    Human UBIAD1 prenyltransferase → Menaquinone-4 biosynthesis source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/k2-research/20953171.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b8786e664d3b32db7b0cca72c710e24f1546e14f0a69c031908400731174cea3", "start_char": 0, "end_char": 2006, "text_sha256": "b8786e664d3b32db7b0cca72c710e24f1546e14f0a69c031908400731174cea3"}
    experimental_model
    Gene knockdown, heterologous expression, isotope conversion and NMR
    exposure
    Labeled vitamin K precursors, UBIAD1 knockdown and expression
    limitations
    Identifies a biosynthetic enzyme, not a clinical requirement to supplement MK-4. K1-derived MK-4 synthesis does not make humans independent of external vitamin K precursors.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Human UBIAD1 in human and insect-cell systems; mouse localization
    plain_language
    Cells have an enzyme that can make MK-4 from vitamin K precursors.
    primary_references
    [k2-p20953171] Identification of UBIAD1 as a novel human menaquinone-4 biosynthetic enzyme. (2010). https://pubmed.ncbi.nlm.nih.gov/20953171/ DOI: 10.1038/nature09464
    tissue_or_cell_type
    MK-4 synthesis

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 136–147

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Gene knockdown, heterologous expression, isotope conversion and NMR · source_derived_draft · unverified_draft

    ### k2-ubiad1-synthesis Human UBIAD1 expression supported conversion of labeled vitamin K precursors to MK-4, identified by deuterium NMR. Condition category: normal nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Cells have an enzyme that can make MK-4 from vitamin K precursors. organism: Human UBIAD1 in human and insect-cell systems; mouse localization tissue_or_cell_type: MK-4 synthesis experimental_model: Gene knockdown, heterologous expression, isotope conversion and NMR limitations: Identifies a biosynthetic enzyme, not a clinical requirement to supplement MK-4. K1-derived MK-4 synthesis does not make humans independent of external vitamin K precursors. exposure: Labeled vitamin K precursors, UBIAD1 knockdown and expression evidence_span: {"source_cache": "artifacts/k2-research/20953171.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b8786e664d3b32db7b0cca72c710e24f1546e14f0a69c031908400731174cea3", "start_char": 0, "end_char": 2006, "text_sha256": "b8786e664d3b32db7b0cca72c710e24f1546e14f0a69c031908400731174cea3"} [k2-p20953171] Identification of UBIAD1 as a novel human menaquinone-4 biosynthetic enzyme. (2010). https://pubmed.ncbi.nlm.nih.gov/20953171/ DOI: 10.1038/nature09464
    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