Component

Vitamin K-dependent coagulation protein function

Vitamin K-dependent coagulation protein function. Species, exposure and limitations are retained in each linked claim.

2 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.

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 acts on it

  1. The GGCX case had combined vitamin K-dependent factor deficiency; vitamin K substitution only partly normalized factor levels.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/k2-research/15287948.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "76e5cf58ebc717968ad3ae32a76aec9f05e783468666181042dfb8989805dadf", "start_char": 0, "end_char": 1069, "text_sha256": "76e5cf58ebc717968ad3ae32a76aec9f05e783468666181042dfb8989805dadf"}
    experimental_model
    Human compound-heterozygous GGCX case and mutation analysis
    exposure
    Splice-site and Arg485Pro variants; vitamin K substitution
    limitations
    Single rare genetic case; the suspected binding-site mechanism was proposed, not established by structure.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Human patient
    plain_language
    The nutrient cannot necessarily repair the protein that uses it.
    primary_references
    [k2-p15287948] Compound heterozygous mutations in the gamma-glutamyl carboxylase gene cause combined deficiency of all vitamin K-dependent blood coagulation factors. (2004). https://pubmed.ncbi.nlm.nih.gov/15287948/ DOI: 10.1111/j.1365-2141.2004.05071.x
    tissue_or_cell_type
    Vitamin K-dependent coagulation proteins
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 929–940

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human compound-heterozygous GGCX case and mutation analysis · source_derived_draft · unverified_draft

    ### k2-ggcx-factor-defect The GGCX case had combined vitamin K-dependent factor deficiency; vitamin K substitution only partly normalized factor levels. Condition category: machinery_impairment nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The nutrient cannot necessarily repair the protein that uses it. organism: Human patient tissue_or_cell_type: Vitamin K-dependent coagulation proteins experimental_model: Human compound-heterozygous GGCX case and mutation analysis limitations: Single rare genetic case; the suspected binding-site mechanism was proposed, not established by structure. exposure: Splice-site and Arg485Pro variants; vitamin K substitution evidence_span: {"source_cache": "artifacts/k2-research/15287948.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "76e5cf58ebc717968ad3ae32a76aec9f05e783468666181042dfb8989805dadf", "start_char": 0, "end_char": 1069, "text_sha256": "76e5cf58ebc717968ad3ae32a76aec9f05e783468666181042dfb8989805dadf"} [k2-p15287948] Compound heterozygous mutations in the gamma-glutamyl carboxylase gene cause combined deficiency of all vitamin K-dependent blood coagulation factors. (2004). https://pubmed.ncbi.nlm.nih.gov/15287948/ DOI: 10.1111/j.1365-2141.2004.05071.x
    Complete structured claim and evidence
  2. Human VKORC1 missense variants were identified in combined vitamin K-dependent factor deficiency and in warfarin resistance; the deficiency variant did not increase VKOR activity upon overexpression.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/k2-research/14765194.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e3691f9cae6d813e59dcad49c9715e4d93db1e6f46d16ec6399f12edb0502e1f", "start_char": 0, "end_char": 1293, "text_sha256": "e3691f9cae6d813e59dcad49c9715e4d93db1e6f46d16ec6399f12edb0502e1f"}
    experimental_model
    Human and rat genetic linkage with functional expression
    exposure
    Inherited deficiency/resistance variants
    limitations
    Rare genetic defects are different from dietary deficiency; historical multiprotein-complex language is not a current structural claim.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Human VKORC1 variants and rat resistance alleles
    plain_language
    Different variants affect either basal function or drug response.
    primary_references
    [k2-p14765194] Mutations in VKORC1 cause warfarin resistance and multiple coagulation factor deficiency type 2. (2004). https://pubmed.ncbi.nlm.nih.gov/14765194/ DOI: 10.1038/nature02214
    tissue_or_cell_type
    Vitamin K recycling and coagulation
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 890–901

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human and rat genetic linkage with functional expression · source_derived_draft · unverified_draft

    ### k2-vkor-human-defect Human VKORC1 missense variants were identified in combined vitamin K-dependent factor deficiency and in warfarin resistance; the deficiency variant did not increase VKOR activity upon overexpression. Condition category: machinery_impairment nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Different variants affect either basal function or drug response. organism: Human VKORC1 variants and rat resistance alleles tissue_or_cell_type: Vitamin K recycling and coagulation experimental_model: Human and rat genetic linkage with functional expression limitations: Rare genetic defects are different from dietary deficiency; historical multiprotein-complex language is not a current structural claim. exposure: Inherited deficiency/resistance variants evidence_span: {"source_cache": "artifacts/k2-research/14765194.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e3691f9cae6d813e59dcad49c9715e4d93db1e6f46d16ec6399f12edb0502e1f", "start_char": 0, "end_char": 1293, "text_sha256": "e3691f9cae6d813e59dcad49c9715e4d93db1e6f46d16ec6399f12edb0502e1f"} [k2-p14765194] Mutations in VKORC1 cause warfarin resistance and multiple coagulation factor deficiency type 2. (2004). https://pubmed.ncbi.nlm.nih.gov/14765194/ DOI: 10.1038/nature02214
    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