Component

Cytochrome P450 26B1 / CYP26B1

Independent protein identity; organism and experimental state are specified on individual claims.

4 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. Recombinant human CYP26B1 formed 4-hydroxy-retinoic acid from all-trans-retinoic acid.

    Cytochrome P450 26B1 / CYP26B1 → 4-Hydroxy-all-trans-retinoic acid source_derived_draftungraded
    Experimental context and source evidence
    evidence_location
    Abstract
    experimental_model
    Human CYP26A1/CYP26B1 expressed in insect cells; purified/reconstituted metabolism and tissue assays.
    exposure
    Substrate series with NADPH and P450 reductase.
    limitations
    Lower in vitro turnover than CYP26A1 does not mean lower importance in every tissue.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Homo sapiens recombinant protein in insect cells
    outcome
    Recombinant human CYP26B1 formed 4-hydroxy-retinoic acid from all-trans-retinoic acid.
    plain_language
    A second independent P450 enzyme also removes the signaling precursor.
    primary_references
    [va-topletz-2012] Comparison of the function and expression of CYP26A1 and CYP26B1, the two retinoic acid hydroxylases (2012). https://pubmed.ncbi.nlm.nih.gov/22020119/ DOI: 10.1016/j.bcp.2011.10.007
    tissue_or_cell_type
    Reconstituted enzyme/microsomes

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 616–628

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human CYP26A1/CYP26B1 expressed in insect cells; purified/reconstituted metabolism and tissue assays. · source_derived_draft · unverified_draft

    ### va-cyp26b1-primary-hydroxylation Recombinant human CYP26B1 formed 4-hydroxy-retinoic acid from all-trans-retinoic acid. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: A second independent P450 enzyme also removes the signaling precursor. organism: Homo sapiens recombinant protein in insect cells tissue_or_cell_type: Reconstituted enzyme/microsomes experimental_model: Human CYP26A1/CYP26B1 expressed in insect cells; purified/reconstituted metabolism and tissue assays. limitations: Lower in vitro turnover than CYP26A1 does not mean lower importance in every tissue. exposure: Substrate series with NADPH and P450 reductase. outcome: Recombinant human CYP26B1 formed 4-hydroxy-retinoic acid from all-trans-retinoic acid. evidence_location: Abstract [va-topletz-2012] Comparison of the function and expression of CYP26A1 and CYP26B1, the two retinoic acid hydroxylases (2012). https://pubmed.ncbi.nlm.nih.gov/22020119/ DOI: 10.1016/j.bcp.2011.10.007
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. CYP26 inhibition with R115866 induced Stra8 in cultured fetal mouse testes.

    R115866 / talarozole → Mouse Stra8 expression source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Embryonic gonad culture
    exposure
    E12.5 testes; 0.7 micromolar R115866 for 2 days.
    limitations
    The inhibitor experiment did not establish bona fide meiotic prophase.
    nutrient_topic
    Vitamin A expansion research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    plain_language
    Local retinoid breakdown restrains the Stra8 response.
    primary_references
    [koubova2006] Retinoic acid regulates sex-specific timing of meiotic initiation in mice. (2006). https://pubmed.ncbi.nlm.nih.gov/16461896/ DOI: 10.1073/pnas.0510813103
    tissue_or_cell_type
    fetal testis

    Vitamin A expansion: reproduction, light-driven vision and shared mechanisms (2026-09-17) · lines 174–185

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Embryonic gonad culture · source_derived_draft · unverified_draft

    ### va-repro-cyp26-inhibitor-stra8 CYP26 inhibition with R115866 induced Stra8 in cultured fetal mouse testes. Condition category: normal nutrient_topic: Vitamin A expansion research collection; topical membership is not evidence of a direct dietary effect. plain_language: Local retinoid breakdown restrains the Stra8 response. organism: Mus musculus tissue_or_cell_type: fetal testis experimental_model: Embryonic gonad culture limitations: The inhibitor experiment did not establish bona fide meiotic prophase. exposure: E12.5 testes; 0.7 micromolar R115866 for 2 days. cross_nutrient: false [koubova2006] Retinoic acid regulates sex-specific timing of meiotic initiation in mice. (2006). https://pubmed.ncbi.nlm.nih.gov/16461896/ DOI: 10.1073/pnas.0510813103
    Complete structured claim and evidence

  2. Cyp26b1-null mouse fetal testes contained germ cells entering meiosis precociously.

    Mouse Cyp26b1 gene → Mouse germ-cell meiotic initiation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Embryonic knockout comparison
    exposure
    Constitutive Cyp26b1 deletion; exact sampling ages unavailable in retrieved abstract.
    limitations
    This establishes a knockout phenotype, not a human RA dose threshold.
    nutrient_topic
    Vitamin A expansion research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    plain_language
    A missing catabolic enzyme disrupts fetal male germ-cell timing.
    primary_references
    [bowles2006] Retinoid signaling determines germ cell fate in mice. (2006). https://pubmed.ncbi.nlm.nih.gov/16574820/ DOI: 10.1126/science.1125691
    tissue_or_cell_type
    fetal testis
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin A expansion: reproduction, light-driven vision and shared mechanisms (2026-09-17) · lines 200–211

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Embryonic knockout comparison · source_derived_draft · unverified_draft

    ### va-repro-cyp26b1-null-meiosis Cyp26b1-null mouse fetal testes contained germ cells entering meiosis precociously. Condition category: machinery_impairment nutrient_topic: Vitamin A expansion research collection; topical membership is not evidence of a direct dietary effect. plain_language: A missing catabolic enzyme disrupts fetal male germ-cell timing. organism: Mus musculus tissue_or_cell_type: fetal testis experimental_model: Embryonic knockout comparison limitations: This establishes a knockout phenotype, not a human RA dose threshold. exposure: Constitutive Cyp26b1 deletion; exact sampling ages unavailable in retrieved abstract. cross_nutrient: false [bowles2006] Retinoid signaling determines germ cell fate in mice. (2006). https://pubmed.ncbi.nlm.nih.gov/16574820/ DOI: 10.1126/science.1125691
    Complete structured claim and evidence

  3. Retinoic acid reduced mineralization in human and murine osteoblast models through RAR-linked effects.

    All-trans-retinoic acid → Osteoblast mineralization source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Retinoid signaling -> calcium/phosphate mineralization.
    experimental_model
    Primary human osteoblasts and MC3T3-E1 cells.
    limitations
    Pharmacology and culture exposure do not define a safe dietary threshold.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Homo sapiens; Mus musculus
    plain_language
    Too much local retinoid signaling can impair mineral deposition in these models.
    primary_references
    [va-lind2013] Vitamin a is a negative regulator of osteoblast mineralization (2013). https://pubmed.ncbi.nlm.nih.gov/24340023/ DOI: 10.1371/journal.pone.0082388
    tissue_or_cell_type
    Osteoblasts

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1650–1660

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary human osteoblasts and MC3T3-E1 cells. · source_derived_draft · unverified_draft

    ### va-retinoic-acid-mineralization Retinoic acid reduced mineralization in human and murine osteoblast models through RAR-linked effects. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Too much local retinoid signaling can impair mineral deposition in these models. organism: Homo sapiens; Mus musculus tissue_or_cell_type: Osteoblasts experimental_model: Primary human osteoblasts and MC3T3-E1 cells. limitations: Pharmacology and culture exposure do not define a safe dietary threshold. cross_nutrient: Retinoid signaling -> calcium/phosphate mineralization. [va-lind2013] Vitamin a is a negative regulator of osteoblast mineralization (2013). https://pubmed.ncbi.nlm.nih.gov/24340023/ DOI: 10.1371/journal.pone.0082388
    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