Component

trans-Urocanate

Context-specific entity; species, compartment and exposure are stated on each claim.

6 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. UV exposure converted trans-urocanic-acid standard to cis isomer; UVB produced faster conversion than UVA under the tested conditions.

    trans-Urocanate → cis-Urocanate source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    In-vitro standards plus analytical measurement of histidine and urocanate isomers in skin washes from eight volunteers.
    limitations
    Photochemistry in standards does not establish a clinical sunscreen effect from oral histidine.
    nutrient_topic
    L-Histidine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Histidine
    plain_language
    Light changes the shape of a histidine-derived skin molecule.
    primary_references
    Determination of histidine and urocanic acid isomers in the human skin by high-performance capillary electrophoresis. · 2000 · https://pubmed.ncbi.nlm.nih.gov/11129077/ · DOI 10.1016/s0378-4347(00)00376-5

    L-Histidine: supply, catabolism, histamine, receptors and cross-nutrient mechanisms (2026-09-19) · lines 434–440

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · In-vitro standards plus analytical measurement of histidine and urocanate isomers in skin washes from eight volunteers. · source_derived_draft · unverified_draft

    ## histidine-urocanate-uv Light changes the shape of a histidine-derived skin molecule. UV exposure converted trans-urocanic-acid standard to cis isomer; UVB produced faster conversion than UVA under the tested conditions. Model: In-vitro standards plus analytical measurement of histidine and urocanate isomers in skin washes from eight volunteers. Limitations: Photochemistry in standards does not establish a clinical sunscreen effect from oral histidine. Evidence access: Primary abstract Determination of histidine and urocanic acid isomers in the human skin by high-performance capillary electrophoresis. · 2000 · https://pubmed.ncbi.nlm.nih.gov/11129077/ · DOI 10.1016/s0378-4347(00)00376-5
    Complete structured claim and evidence

What acts on it

  1. HAL initiates histidine degradation by converting L-histidine to trans-urocanate with ammonia release.

    Human histidine ammonia-lyase / HAL → trans-Urocanate source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text; pathway background
    experimental_model
    Established reaction in the pathway map of a primary human cancer-cell study; genetic perturbation and metabolomics investigate pathway flux rather than purified kinetics of every individual enzyme.
    limitations
    Reaction background is distinguished from the study-specific CRISPR findings below. Correction record: A 2022 author correction is indexed (PMID 35017686). The publisher-accessible record identifies corrected Fig. 1f, Extended Data Fig. 11, Supplementary Fig. 3 and source data for Figs. 1/2, including an erroneous doxorubicin replicate. Complete correction narrative was not accessible; its full impact is not independently cleared. The original study remains flagged corrected, and no comprehensive safety claim is made. https://www.nature.com/articles/s41586-021-03487-2
    nutrient_topic
    L-Histidine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Histidine
    plain_language
    The first breakdown enzyme directs histidine toward urocanate.
    primary_references
    Histidine catabolism is a major determinant of methotrexate sensitivity. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29995852/ · DOI 10.1038/s41586-018-0316-7

    L-Histidine: supply, catabolism, histamine, receptors and cross-nutrient mechanisms (2026-09-19) · lines 106–112

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Established reaction in the pathway map of a primary human cancer-cell study; genetic perturbation and metabolomics investigate pathway flux rather than purified kinetics of every individual enzyme. · source_derived_draft · unverified_draft

    ## histidine-hal-reaction The first breakdown enzyme directs histidine toward urocanate. HAL initiates histidine degradation by converting L-histidine to trans-urocanate with ammonia release. Model: Established reaction in the pathway map of a primary human cancer-cell study; genetic perturbation and metabolomics investigate pathway flux rather than purified kinetics of every individual enzyme. Limitations: Reaction background is distinguished from the study-specific CRISPR findings below. Correction record: A 2022 author correction is indexed (PMID 35017686). The publisher-accessible record identifies corrected Fig. 1f, Extended Data Fig. 11, Supplementary Fig. 3 and source data for Figs. 1/2, including an erroneous doxorubicin replicate. Complete correction narrative was not accessible; its full impact is not independently cleared. The original study remains flagged corrected, and no comprehensive safety claim is made. https://www.nature.com/articles/s41586-021-03487-2 Evidence access: Primary full text; pathway background Histidine catabolism is a major determinant of methotrexate sensitivity. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29995852/ · DOI 10.1038/s41586-018-0316-7
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. The UrdA catalytic-domain structures contained FAD alongside substrate or product, and assays supported flavin-associated urocanate reduction.

    FAD → Shewanella oneidensis MR-1 urocanate reductase / UrdA source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Bacterial structural enzymology; FAD-supplemented enzyme assays.
    limitations
    Does not show that human riboflavin intake limits or increases microbial imidazole-propionate production.
    nutrient_topic
    L-Histidine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Histidine
    plain_language
    This microbial reaction uses a riboflavin-derived chemical tool.
    primary_references
    Structural characterization of the microbial enzyme urocanate reductase mediating imidazole propionate production. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33649331/ · DOI 10.1038/s41467-021-21548-y

    L-Histidine: supply, catabolism, histamine, receptors and cross-nutrient mechanisms (2026-09-19) · lines 274–280

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Bacterial structural enzymology; FAD-supplemented enzyme assays. · source_derived_draft · unverified_draft

    ## histidine-urda-flavin This microbial reaction uses a riboflavin-derived chemical tool. The UrdA catalytic-domain structures contained FAD alongside substrate or product, and assays supported flavin-associated urocanate reduction. Model: Bacterial structural enzymology; FAD-supplemented enzyme assays. Limitations: Does not show that human riboflavin intake limits or increases microbial imidazole-propionate production. Evidence access: Primary full text Structural characterization of the microbial enzyme urocanate reductase mediating imidazole propionate production. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33649331/ · DOI 10.1038/s41467-021-21548-y
    Complete structured claim and evidence

  2. Full-length and two-domain S. oneidensis UrdA converted urocanate to imidazole propionate and did not show the tested fumarate-reductase activity.

    Shewanella oneidensis MR-1 urocanate reductase / UrdA → Imidazole propionate source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Purified bacterial full-length/truncated proteins, activity assays and ligand-bound crystal structures.
    limitations
    This species is a structural model; abundance or flux in an individual human microbiome is not measured.
    nutrient_topic
    L-Histidine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Histidine
    plain_language
    A bacterial enzyme sends a histidine-derived intermediate down a different branch.
    primary_references
    Structural characterization of the microbial enzyme urocanate reductase mediating imidazole propionate production. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33649331/ · DOI 10.1038/s41467-021-21548-y

    L-Histidine: supply, catabolism, histamine, receptors and cross-nutrient mechanisms (2026-09-19) · lines 266–272

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Purified bacterial full-length/truncated proteins, activity assays and ligand-bound crystal structures. · source_derived_draft · unverified_draft

    ## histidine-urda-product A bacterial enzyme sends a histidine-derived intermediate down a different branch. Full-length and two-domain S. oneidensis UrdA converted urocanate to imidazole propionate and did not show the tested fumarate-reductase activity. Model: Purified bacterial full-length/truncated proteins, activity assays and ligand-bound crystal structures. Limitations: This species is a structural model; abundance or flux in an individual human microbiome is not measured. Evidence access: Primary full text Structural characterization of the microbial enzyme urocanate reductase mediating imidazole propionate production. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33649331/ · DOI 10.1038/s41467-021-21548-y
    Complete structured claim and evidence

  3. A girl with urocanic aciduria carried UROC1 L70P/R450C variants; expression and activity studies supported impaired enzyme function.

    Human urocanate hydratase / UROC1 → Urocanate handling in human UROC1-associated aciduria source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Single human case plus variant expression, enzyme assays and computational interpretation.
    limitations
    The biochemical association is stronger than attribution of every neurological feature in a single patient.
    nutrient_topic
    L-Histidine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Histidine
    plain_language
    A block at the second enzyme allowed an upstream metabolite to accumulate.
    primary_references
    Mutations in the urocanase gene UROC1 are associated with urocanic aciduria. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19304569/ · DOI 10.1136/jmg.2008.060632
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Histidine: supply, catabolism, histamine, receptors and cross-nutrient mechanisms (2026-09-19) · lines 186–192

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Single human case plus variant expression, enzyme assays and computational interpretation. · source_derived_draft · unverified_draft

    ## histidine-uroc-human-loss A block at the second enzyme allowed an upstream metabolite to accumulate. A girl with urocanic aciduria carried UROC1 L70P/R450C variants; expression and activity studies supported impaired enzyme function. Model: Single human case plus variant expression, enzyme assays and computational interpretation. Limitations: The biochemical association is stronger than attribution of every neurological feature in a single patient. Evidence access: Primary abstract Mutations in the urocanase gene UROC1 are associated with urocanic aciduria. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19304569/ · DOI 10.1136/jmg.2008.060632
    Complete structured claim and evidence

  4. UROC1 hydrates urocanate to imidazolonepropionate in the histidine degradation pathway.

    Human urocanate hydratase / UROC1 → 4-Imidazolone-5-propionate source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text; pathway background
    experimental_model
    Established reaction in the pathway map of a primary human cancer-cell study; genetic perturbation and metabolomics investigate pathway flux rather than purified kinetics of every individual enzyme.
    limitations
    Not a claim that added histidine can bypass UROC1 loss. Correction record: A 2022 author correction is indexed (PMID 35017686). The publisher-accessible record identifies corrected Fig. 1f, Extended Data Fig. 11, Supplementary Fig. 3 and source data for Figs. 1/2, including an erroneous doxorubicin replicate. Complete correction narrative was not accessible; its full impact is not independently cleared. The original study remains flagged corrected, and no comprehensive safety claim is made. https://www.nature.com/articles/s41586-021-03487-2
    nutrient_topic
    L-Histidine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Histidine
    plain_language
    A second enzyme changes urocanate into the next intermediate.
    primary_references
    Histidine catabolism is a major determinant of methotrexate sensitivity. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29995852/ · DOI 10.1038/s41586-018-0316-7

    L-Histidine: supply, catabolism, histamine, receptors and cross-nutrient mechanisms (2026-09-19) · lines 114–120

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Established reaction in the pathway map of a primary human cancer-cell study; genetic perturbation and metabolomics investigate pathway flux rather than purified kinetics of every individual enzyme. · source_derived_draft · unverified_draft

    ## histidine-uroc-reaction A second enzyme changes urocanate into the next intermediate. UROC1 hydrates urocanate to imidazolonepropionate in the histidine degradation pathway. Model: Established reaction in the pathway map of a primary human cancer-cell study; genetic perturbation and metabolomics investigate pathway flux rather than purified kinetics of every individual enzyme. Limitations: Not a claim that added histidine can bypass UROC1 loss. Correction record: A 2022 author correction is indexed (PMID 35017686). The publisher-accessible record identifies corrected Fig. 1f, Extended Data Fig. 11, Supplementary Fig. 3 and source data for Figs. 1/2, including an erroneous doxorubicin replicate. Complete correction narrative was not accessible; its full impact is not independently cleared. The original study remains flagged corrected, and no comprehensive safety claim is made. https://www.nature.com/articles/s41586-021-03487-2 Evidence access: Primary full text; pathway background Histidine catabolism is a major determinant of methotrexate sensitivity. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29995852/ · DOI 10.1038/s41586-018-0316-7
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

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