Component

Mouse Camp mRNA

Study-defined Mouse Camp mRNA. Read each linked record for species, exposure and endpoint.

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.

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. CAMP induction was not observed in the tested murine cells; the primate-conserved promoter VDRE was absent from mouse, rat and canine genomes.

    Calcitriol → Mouse Camp mRNA source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Human cell lines and bone-marrow-derived cells; promoter studies and mouse comparison
    exposure
    Murine cell response and comparative promoter analysis.
    limitations
    Species boundary, not proof that vitamin D has no immune actions in rodents.
    nutrient_topic
    Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
    organism
    Mus musculus; comparative mammalian DNA
    plain_language
    This human antimicrobial gene-control route cannot simply be copied into a mouse model.
    primary_references
    [gombart2005] Human cathelicidin antimicrobial peptide (CAMP) gene is a direct target of the vitamin D receptor and is strongly up-regulated in myeloid cells by 1,25-dihydroxyvitamin D3. (2005). https://pubmed.ncbi.nlm.nih.gov/15985530/ DOI: 10.1096/fj.04-3284com
    tissue_or_cell_type
    Murine cells and comparative promoter sequences

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 931–942

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human cell lines and bone-marrow-derived cells; promoter studies and mouse comparison · source_derived_draft · unverified_draft

    ### vd-camp-mouse-boundary CAMP induction was not observed in the tested murine cells; the primate-conserved promoter VDRE was absent from mouse, rat and canine genomes. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: This human antimicrobial gene-control route cannot simply be copied into a mouse model. organism: Mus musculus; comparative mammalian DNA tissue_or_cell_type: Murine cells and comparative promoter sequences experimental_model: Human cell lines and bone-marrow-derived cells; promoter studies and mouse comparison limitations: Species boundary, not proof that vitamin D has no immune actions in rodents. exposure: Murine cell response and comparative promoter analysis. cross_nutrient: false [gombart2005] Human cathelicidin antimicrobial peptide (CAMP) gene is a direct target of the vitamin D receptor and is strongly up-regulated in myeloid cells by 1,25-dihydroxyvitamin D3. (2005). https://pubmed.ncbi.nlm.nih.gov/15985530/ DOI: 10.1096/fj.04-3284com
    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