Component

Prothrombin / coagulation factor II / F2

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

5 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. Factor Xa activated bovine prothrombin efficiently when factor Va, Ca2+ and phosphatidylserine-containing phospholipids assembled the complete prothrombinase system.

    Prothrombin / coagulation factor II / F2 → Thrombin (proteolytically activated F2) source_derived_draftungraded
    Experimental context and source evidence
    compartment_description
    Phospholipid surface
    experimental_model
    Kinetic reconstitution with defined phospholipids
    limitations
    Low residual Xa activity exists without the complete complex; this establishes biochemical assistance, not that extra dietary calcium accelerates clotting.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Bos taurus
    plain_language
    Calcium helps the membrane-associated clotting machinery generate thrombin.
    primary_references
    [rosing1980] The role of phospholipids and factor Va in the prothrombinase complex (1980). https://pubmed.ncbi.nlm.nih.gov/7350159/ DOI: 10.1016/S0021-9258(19)86294-4
    tissue_or_cell_type
    Purified blood proteins

    Calcium: mechanism-first literature curation (2026-09-17) · lines 1116–1126

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Kinetic reconstitution with defined phospholipids · source_derived_draft · unverified_draft

    ### calcium-phospholipid-prothrombinase Factor Xa activated bovine prothrombin efficiently when factor Va, Ca2+ and phosphatidylserine-containing phospholipids assembled the complete prothrombinase system. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Calcium helps the membrane-associated clotting machinery generate thrombin. organism: Bos taurus tissue_or_cell_type: Purified blood proteins experimental_model: Kinetic reconstitution with defined phospholipids limitations: Low residual Xa activity exists without the complete complex; this establishes biochemical assistance, not that extra dietary calcium accelerates clotting. compartment_description: Phospholipid surface [rosing1980] The role of phospholipids and factor Va in the prothrombinase complex (1980). https://pubmed.ncbi.nlm.nih.gov/7350159/ DOI: 10.1016/S0021-9258(19)86294-4
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. In the bovine prothrombin Gla-domain structure, the lysophosphatidylserine headgroup contacted domain-bound Ca2+ and gamma-carboxyglutamate residues.

    Calcium ion → Gamma-carboxylated prothrombin Gla domain source_derived_draftungraded
    Experimental context and source evidence
    compartment_description
    Extracellular protein-membrane interface
    experimental_model
    X-ray crystallography and NMR with lysophosphatidylserine
    limitations
    The carboxylated Gla domain is a vitamin-K-dependent protein state; calcium binding does not perform gamma-carboxylation.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Bos taurus
    plain_language
    Protein-bound calcium helps a clotting protein recognize a membrane lipid headgroup.
    primary_references
    [huang2003] Structural basis of membrane binding by Gla domains of vitamin K-dependent proteins (2003). https://www.nature.com/articles/nsb971 DOI: 10.1038/nsb971
    tissue_or_cell_type
    Purified prothrombin fragment; blood-protein context

    Calcium: mechanism-first literature curation (2026-09-17) · lines 1104–1114

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · X-ray crystallography and NMR with lysophosphatidylserine · source_derived_draft · unverified_draft

    ### calcium-gla-phosphatidylserine-binding In the bovine prothrombin Gla-domain structure, the lysophosphatidylserine headgroup contacted domain-bound Ca2+ and gamma-carboxyglutamate residues. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Protein-bound calcium helps a clotting protein recognize a membrane lipid headgroup. organism: Bos taurus tissue_or_cell_type: Purified prothrombin fragment; blood-protein context experimental_model: X-ray crystallography and NMR with lysophosphatidylserine limitations: The carboxylated Gla domain is a vitamin-K-dependent protein state; calcium binding does not perform gamma-carboxylation. compartment_description: Extracellular protein-membrane interface [huang2003] Structural basis of membrane binding by Gla domains of vitamin K-dependent proteins (2003). https://www.nature.com/articles/nsb971 DOI: 10.1038/nsb971
    Complete structured claim and evidence

  2. 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

  3. 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

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

    Gamma-glutamyl carboxylase / GGCX → Vitamin K-dependent coagulation protein function source_derived_draftungraded
    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

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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