Component

Human peptide/histidine transporter PHT1 / SLC15A4

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

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. Human SLC15A4 interacted with TASL and was required for its endolysosomal localization and function in the tested cells.

    Human peptide/histidine transporter PHT1 / SLC15A4 → Human TLR adaptor interacting with SLC15A4 / TASL source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Primary and transformed human immune cells; interaction mapping and mutagenesis.
    limitations
    Docking does not prove that the amount of histidine transported is the limiting signal.
    nutrient_topic
    L-Histidine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Histidine
    plain_language
    The transporter also serves as a docking location for a signaling adaptor.
    primary_references
    TASL is the SLC15A4-associated adaptor for IRF5 activation by TLR7-9. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32433612/ · DOI 10.1038/s41586-020-2282-0

    L-Histidine: supply, catabolism, histamine, receptors and cross-nutrient mechanisms (2026-09-19) · lines 378–384

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Primary and transformed human immune cells; interaction mapping and mutagenesis. · source_derived_draft · unverified_draft

    ## histidine-tasl-recruitment The transporter also serves as a docking location for a signaling adaptor. Human SLC15A4 interacted with TASL and was required for its endolysosomal localization and function in the tested cells. Model: Primary and transformed human immune cells; interaction mapping and mutagenesis. Limitations: Docking does not prove that the amount of histidine transported is the limiting signal. Evidence access: Primary full text TASL is the SLC15A4-associated adaptor for IRF5 activation by TLR7-9. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32433612/ · DOI 10.1038/s41586-020-2282-0
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Artificially tethering TASL to endolysosomes restored TLR7-9-induced IRF5 activation and interferon/cytokine production in SLC15A4-deficient human cells.

    Human TLR adaptor interacting with SLC15A4 / TASL → Human endolysosomal TLR IRF signaling source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Engineered human-cell localization/rescue experiments.
    limitations
    Shows transport is dispensable with this bypass; does not show native transport is irrelevant in every cell, or replicate mouse IRF7 experiments under identical conditions.
    nutrient_topic
    L-Histidine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Histidine
    plain_language
    A targeted scaffold bypass restored signaling without the transporter.
    primary_references
    SLC15A4 controls endolysosomal TLR7-9 responses by recruiting the innate immune adaptor TASL. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37527038/ · DOI 10.1016/j.celrep.2023.112916
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Histidine: supply, catabolism, histamine, receptors and cross-nutrient mechanisms (2026-09-19) · lines 402–408

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Engineered human-cell localization/rescue experiments. · source_derived_draft · unverified_draft

    ## histidine-tasl-bypass A targeted scaffold bypass restored signaling without the transporter. Artificially tethering TASL to endolysosomes restored TLR7-9-induced IRF5 activation and interferon/cytokine production in SLC15A4-deficient human cells. Model: Engineered human-cell localization/rescue experiments. Limitations: Shows transport is dispensable with this bypass; does not show native transport is irrelevant in every cell, or replicate mouse IRF7 experiments under identical conditions. Evidence access: Primary abstract SLC15A4 controls endolysosomal TLR7-9 responses by recruiting the innate immune adaptor TASL. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37527038/ · DOI 10.1016/j.celrep.2023.112916
    Complete structured claim and evidence

  2. The conserved TASL pLxIS motif mediated recruitment and activation of IRF5 downstream of endolysosomal TLR7/8/9 stimulation.

    Human TLR adaptor interacting with SLC15A4 / TASL → Human interferon regulatory factor 5 / IRF5 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Human immune-cell mutagenesis and signaling experiments.
    limitations
    A shared transporter node does not establish a nutritional intervention.
    nutrient_topic
    L-Histidine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Histidine
    plain_language
    An adaptor connects the membrane-associated system to a transcription factor.
    primary_references
    TASL is the SLC15A4-associated adaptor for IRF5 activation by TLR7-9. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32433612/ · DOI 10.1038/s41586-020-2282-0

    L-Histidine: supply, catabolism, histamine, receptors and cross-nutrient mechanisms (2026-09-19) · lines 386–392

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human immune-cell mutagenesis and signaling experiments. · source_derived_draft · unverified_draft

    ## histidine-tasl-irf5 An adaptor connects the membrane-associated system to a transcription factor. The conserved TASL pLxIS motif mediated recruitment and activation of IRF5 downstream of endolysosomal TLR7/8/9 stimulation. Model: Human immune-cell mutagenesis and signaling experiments. Limitations: A shared transporter node does not establish a nutritional intervention. Evidence access: Primary full text TASL is the SLC15A4-associated adaptor for IRF5 activation by TLR7-9. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32433612/ · DOI 10.1038/s41586-020-2282-0
    Complete structured claim and evidence

  3. Deleting TASL or SLC15A4 impaired the IRF response without abolishing the measured NF-kappaB or MAPK responses.

    Human TLR adaptor interacting with SLC15A4 / TASL → Human endolysosomal TLR IRF signaling source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Human immune-cell deletion experiments.
    limitations
    Does not imply all immune function is lost or a global histidine shortage.
    nutrient_topic
    L-Histidine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Histidine
    plain_language
    Loss of the system selectively disrupted one signaling branch.
    primary_references
    TASL is the SLC15A4-associated adaptor for IRF5 activation by TLR7-9. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32433612/ · DOI 10.1038/s41586-020-2282-0
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Histidine: supply, catabolism, histamine, receptors and cross-nutrient mechanisms (2026-09-19) · lines 394–400

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human immune-cell deletion experiments. · source_derived_draft · unverified_draft

    ## histidine-tasl-loss-selectivity Loss of the system selectively disrupted one signaling branch. Deleting TASL or SLC15A4 impaired the IRF response without abolishing the measured NF-kappaB or MAPK responses. Model: Human immune-cell deletion experiments. Limitations: Does not imply all immune function is lost or a global histidine shortage. Evidence access: Primary full text TASL is the SLC15A4-associated adaptor for IRF5 activation by TLR7-9. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32433612/ · DOI 10.1038/s41586-020-2282-0
    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