Component
Human protein Z / PROZ
Human protein Z / PROZ. Species, exposure and limitations are retained in each linked claim.
1 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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
Where it participates (unsigned role)
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
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.