Component

Mouse pregnane X receptor / Pxr / Nr1i2

Mouse pregnane X receptor / Pxr / Nr1i2. Species, exposure and limitations are retained in each linked claim.

3 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 it acts on

  1. Vitamin K2 induced bone-marker expression in wild-type mouse calvarial cells but not Pxr-deficient cells.

    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
    The measured outcome was expression of bone markers, not actual mineral deposition; loss of the mouse receptor need not predict human supplement response.
    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
    The transcriptional response depended on the receptor in this model.
    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 708–719

    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-mouse-pxr-dependence Vitamin K2 induced bone-marker expression in wild-type mouse calvarial cells but not Pxr-deficient cells. Condition category: normal nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The transcriptional response depended on the receptor in this model. 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: The measured outcome was expression of bone markers, not actual mineral deposition; loss of the mouse receptor need not predict human supplement response. 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
  2. Nr1i2-deficient mice had a barrier defect with increased TLR4-related signaling; additional Tlr4 deletion corrected the permeability phenotype.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text, genetic barrier experiments
    experimental_model
    Mouse Nr1i2 and Tlr4 genetic perturbations.
    limitations
    Does not demonstrate the same causal chain in human patients.
    nutrient_topic
    Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
    plain_language
    Receptor status and inflammatory sensing determined the barrier outcome.
    primary_references
    Symbiotic bacterial metabolites regulate gastrointestinal barrier function via the xenobiotic sensor PXR and Toll-like receptor 4. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25065623/ · DOI 10.1016/j.immuni.2014.06.014
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 538–544

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse Nr1i2 and Tlr4 genetic perturbations. · source_derived_draft · unverified_draft

    ## tryptophan-pxr-tlr4-barrier Receptor status and inflammatory sensing determined the barrier outcome. Nr1i2-deficient mice had a barrier defect with increased TLR4-related signaling; additional Tlr4 deletion corrected the permeability phenotype. Model: Mouse Nr1i2 and Tlr4 genetic perturbations. Limitations: Does not demonstrate the same causal chain in human patients. Evidence access: Primary full text, genetic barrier experiments Symbiotic bacterial metabolites regulate gastrointestinal barrier function via the xenobiotic sensor PXR and Toll-like receptor 4. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25065623/ · DOI 10.1016/j.immuni.2014.06.014
    Complete structured claim and evidence

What acts on it

  1. Indolepropionate activated mouse PXR with an EC50 near 0.55 micromolar in the reporter assay.

    Experimental context and source evidence
    evidence_access
    Primary full text, Figure 1
    experimental_model
    Mouse PXR expressed in 293T cells.
    limitations
    Expression host does not make the receptor human; potency differed sharply for human PXR.
    nutrient_topic
    Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
    plain_language
    The mouse receptor was sensitive to this microbial product.
    primary_references
    Symbiotic bacterial metabolites regulate gastrointestinal barrier function via the xenobiotic sensor PXR and Toll-like receptor 4. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25065623/ · DOI 10.1016/j.immuni.2014.06.014

    Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 522–528

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse PXR expressed in 293T cells. · source_derived_draft · unverified_draft

    ## tryptophan-ipa-mouse-pxr The mouse receptor was sensitive to this microbial product. Indolepropionate activated mouse PXR with an EC50 near 0.55 micromolar in the reporter assay. Model: Mouse PXR expressed in 293T cells. Limitations: Expression host does not make the receptor human; potency differed sharply for human PXR. Evidence access: Primary full text, Figure 1 Symbiotic bacterial metabolites regulate gastrointestinal barrier function via the xenobiotic sensor PXR and Toll-like receptor 4. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25065623/ · DOI 10.1016/j.immuni.2014.06.014
    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