Component

Mouse 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. Deleting Pht1 reduced histidine uptake in mouse brain slices by about half; Pept2 expression increased approximately twofold.

    Mouse peptide/histidine transporter Pht1 / Slc15a4 → Histidine uptake into mouse brain slices source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Pht1-null and matched wild-type adult mice; brain slices and transporter expression.
    limitations
    Genetic deletion is not dietary histidine deficiency.
    nutrient_topic
    L-Histidine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Histidine
    plain_language
    Loss of one transporter altered uptake even with a compensatory response.
    primary_references
    A novel role for PHT1 in the disposition of l-histidine in brain: In vitro slice and in vivo pharmacokinetic studies in wildtype and Pht1 null mice. · 2017 · https://pubmed.ncbi.nlm.nih.gov/27845049/ · DOI 10.1016/j.bcp.2016.11.012
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Histidine: supply, catabolism, histamine, receptors and cross-nutrient mechanisms (2026-09-19) · lines 90–96

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Pht1-null and matched wild-type adult mice; brain slices and transporter expression. · source_derived_draft · unverified_draft

    ## histidine-pht1-brain-uptake Loss of one transporter altered uptake even with a compensatory response. Deleting Pht1 reduced histidine uptake in mouse brain slices by about half; Pept2 expression increased approximately twofold. Model: Pht1-null and matched wild-type adult mice; brain slices and transporter expression. Limitations: Genetic deletion is not dietary histidine deficiency. Evidence access: Primary full text A novel role for PHT1 in the disposition of l-histidine in brain: In vitro slice and in vivo pharmacokinetic studies in wildtype and Pht1 null mice. · 2017 · https://pubmed.ncbi.nlm.nih.gov/27845049/ · DOI 10.1016/j.bcp.2016.11.012
    Complete structured claim and evidence

  2. Five minutes after intravenous histidine, Pht1-null mouse brain parenchyma contained 28-48 percent less tracer-associated histidine than wild type, despite comparable plasma time courses and no corresponding CSF difference.

    Mouse peptide/histidine transporter Pht1 / Slc15a4 → Brain-parenchymal histidine after intravenous dosing source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse knockout and intravenous pharmacokinetics.
    limitations
    Acute tracer distribution cannot define steady-state human brain deficiency.
    nutrient_topic
    L-Histidine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Histidine
    plain_language
    A normal circulating profile did not guarantee the same tissue exposure.
    primary_references
    A novel role for PHT1 in the disposition of l-histidine in brain: In vitro slice and in vivo pharmacokinetic studies in wildtype and Pht1 null mice. · 2017 · https://pubmed.ncbi.nlm.nih.gov/27845049/ · DOI 10.1016/j.bcp.2016.11.012
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Histidine: supply, catabolism, histamine, receptors and cross-nutrient mechanisms (2026-09-19) · lines 98–104

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse knockout and intravenous pharmacokinetics. · source_derived_draft · unverified_draft

    ## histidine-pht1-compartments A normal circulating profile did not guarantee the same tissue exposure. Five minutes after intravenous histidine, Pht1-null mouse brain parenchyma contained 28-48 percent less tracer-associated histidine than wild type, despite comparable plasma time courses and no corresponding CSF difference. Model: Mouse knockout and intravenous pharmacokinetics. Limitations: Acute tracer distribution cannot define steady-state human brain deficiency. Evidence access: Primary full text A novel role for PHT1 in the disposition of l-histidine in brain: In vitro slice and in vivo pharmacokinetic studies in wildtype and Pht1 null mice. · 2017 · https://pubmed.ncbi.nlm.nih.gov/27845049/ · DOI 10.1016/j.bcp.2016.11.012
    Complete structured claim and evidence

  3. Mouse experiments attributed TLR-triggered cytokine production to functional Slc15a4 transport and linked Slc15a4 loss with reduced pathogenic antibody production.

    Mouse peptide/histidine transporter Pht1 / Slc15a4 → TLR7-induced interferon and antibody output in mouse B cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Mouse genetic/transport-function study.
    limitations
    Later human TASL-tethering experiments provide a scaffold bypass; this is not proof that dietary histidine controls autoimmunity.
    nutrient_topic
    L-Histidine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Histidine
    plain_language
    The original model linked transporter function with the immune response.
    primary_references
    The histidine transporter SLC15A4 coordinates mTOR-dependent inflammatory responses and pathogenic antibody production. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25238095/ · DOI 10.1016/j.immuni.2014.08.011
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Histidine: supply, catabolism, histamine, receptors and cross-nutrient mechanisms (2026-09-19) · lines 370–376

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse genetic/transport-function study. · source_derived_draft · unverified_draft

    ## histidine-slc15a4-mouse-cytokines The original model linked transporter function with the immune response. Mouse experiments attributed TLR-triggered cytokine production to functional Slc15a4 transport and linked Slc15a4 loss with reduced pathogenic antibody production. Model: Mouse genetic/transport-function study. Limitations: Later human TASL-tethering experiments provide a scaffold bypass; this is not proof that dietary histidine controls autoimmunity. Evidence access: Primary abstract The histidine transporter SLC15A4 coordinates mTOR-dependent inflammatory responses and pathogenic antibody production. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25238095/ · DOI 10.1016/j.immuni.2014.08.011
    Complete structured claim and evidence

  4. Slc15a4 loss disturbed mouse B-cell endolysosomal pH regulation and was associated with disrupted mTOR signaling and the IRF7/type-I-interferon circuit.

    Mouse peptide/histidine transporter Pht1 / Slc15a4 → Endolysosomal pH regulation in mouse B cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Mouse B-cell genetic experiments and lupus model.
    limitations
    v-ATPase integrity was proposed rather than definitively established as the sole cause. Histidine intake was not the manipulation.
    nutrient_topic
    L-Histidine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Histidine
    plain_language
    Losing a transporter-associated system changed the local organelle environment and immune signaling.
    primary_references
    The histidine transporter SLC15A4 coordinates mTOR-dependent inflammatory responses and pathogenic antibody production. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25238095/ · DOI 10.1016/j.immuni.2014.08.011
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Histidine: supply, catabolism, histamine, receptors and cross-nutrient mechanisms (2026-09-19) · lines 362–368

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse B-cell genetic experiments and lupus model. · source_derived_draft · unverified_draft

    ## histidine-slc15a4-mouse-ph Losing a transporter-associated system changed the local organelle environment and immune signaling. Slc15a4 loss disturbed mouse B-cell endolysosomal pH regulation and was associated with disrupted mTOR signaling and the IRF7/type-I-interferon circuit. Model: Mouse B-cell genetic experiments and lupus model. Limitations: v-ATPase integrity was proposed rather than definitively established as the sole cause. Histidine intake was not the manipulation. Evidence access: Primary abstract The histidine transporter SLC15A4 coordinates mTOR-dependent inflammatory responses and pathogenic antibody production. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25238095/ · DOI 10.1016/j.immuni.2014.08.011
    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.

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