Component

Keratinocyte-targeted ligand-binding-defective VDR transgene

Study-defined Keratinocyte-targeted ligand-binding-defective VDR transgene. 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 it acts on

  1. Keratinocyte-targeted ligand-binding-defective VDR restored normal hair cycling in VDR-null mice.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Keratinocyte-targeted mutant VDR transgenes in VDR-null mice; binding/repression assays
    exposure
    Keratinocyte-specific mutant VDR transgenes in VDR-null mice.
    limitations
    Engineered mouse VDR system; does not establish a vitamin D supplement as treatment for human hair loss.
    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
    plain_language
    A receptor defect and a vitamin shortage are different problems.
    primary_references
    [skorija2005] Ligand-independent actions of the vitamin D receptor maintain hair follicle homeostasis. (2005). https://pubmed.ncbi.nlm.nih.gov/15591533/ DOI: 10.1210/me.2004-0415
    tissue_or_cell_type
    Keratinocytes/hair follicles
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1184–1195

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Keratinocyte-targeted mutant VDR transgenes in VDR-null mice; binding/repression assays · source_derived_draft · unverified_draft

    ### vd-hair-binding Keratinocyte-targeted ligand-binding-defective VDR restored normal hair cycling in VDR-null mice. Condition category: machinery_impairment nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A receptor defect and a vitamin shortage are different problems. organism: Mus musculus tissue_or_cell_type: Keratinocytes/hair follicles experimental_model: Keratinocyte-targeted mutant VDR transgenes in VDR-null mice; binding/repression assays limitations: Engineered mouse VDR system; does not establish a vitamin D supplement as treatment for human hair loss. exposure: Keratinocyte-specific mutant VDR transgenes in VDR-null mice. cross_nutrient: false [skorija2005] Ligand-independent actions of the vitamin D receptor maintain hair follicle homeostasis. (2005). https://pubmed.ncbi.nlm.nih.gov/15591533/ DOI: 10.1210/me.2004-0415
    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