Component

Human taste receptor TAS1R1

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

5 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/mouse receptor chimeras and point mutants mapped acidic-amino-acid selectivity to the T1R1 ligand-binding region and identified other residues that broadened mouse-type responses.

    Human taste receptor TAS1R1 → Human umami receptor TAS1R1/TAS1R3 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Human/mouse receptor chimeras and mutagenesis.
    limitations
    Sequence-dependent selectivity is not evidence that all mammalian umami receptors behave identically.
    nutrient_topic
    L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
    plain_language
    The species of the receptor changes what the same ligand experiment means.
    primary_references
    Two distinct determinants of ligand specificity in T1R1/T1R3 (the umami taste receptor). · 2013 · https://pubmed.ncbi.nlm.nih.gov/24214976/ · DOI 10.1074/jbc.M113.494443

    L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19) · lines 58–64

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human/mouse receptor chimeras and mutagenesis. · source_derived_draft · unverified_draft

    ## glutamate-umami-species The species of the receptor changes what the same ligand experiment means. Human/mouse receptor chimeras and point mutants mapped acidic-amino-acid selectivity to the T1R1 ligand-binding region and identified other residues that broadened mouse-type responses. Model: Human/mouse receptor chimeras and mutagenesis. Limitations: Sequence-dependent selectivity is not evidence that all mammalian umami receptors behave identically. Evidence access: Primary full text Two distinct determinants of ligand specificity in T1R1/T1R3 (the umami taste receptor). · 2013 · https://pubmed.ncbi.nlm.nih.gov/24214976/ · DOI 10.1074/jbc.M113.494443
    Complete structured claim and evidence

What acts on it

  1. The cooperative model places a 5-prime-ribonucleotide at an adjacent opening-side site, stabilizing the closed glutamate-bound receptor conformation.

    Inosine 5-prime-monophosphate / IMP → Human taste receptor TAS1R1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Same mutagenesis/chimera/model study.
    limitations
    Do not extrapolate taste synergy to a general systemic metabolic benefit.
    nutrient_topic
    Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
    plain_language
    IMP can amplify a glutamate signal through a different receptor contact.
    primary_references
    Molecular mechanism for the umami taste synergism. · 2008 · https://pubmed.ncbi.nlm.nih.gov/19104071/ · DOI 10.1073/pnas.0810174106

    Monosodium Glutamate (MSG): taste, gut sensing, exposure and cross-nutrient mechanisms (2026-09-20) · lines 82–88

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Same mutagenesis/chimera/model study. · source_derived_draft · unverified_draft

    ## monosodium-glutamate-imp-cooperation IMP can amplify a glutamate signal through a different receptor contact. The cooperative model places a 5-prime-ribonucleotide at an adjacent opening-side site, stabilizing the closed glutamate-bound receptor conformation. Model: Same mutagenesis/chimera/model study. Limitations: Do not extrapolate taste synergy to a general systemic metabolic benefit. Evidence access: Primary abstract Molecular mechanism for the umami taste synergism. · 2008 · https://pubmed.ncbi.nlm.nih.gov/19104071/ · DOI 10.1073/pnas.0810174106
    Complete structured claim and evidence

  2. Receptor chimeras, mutagenesis and modeling support glutamate binding near the hinge of the T1R1 Venus-flytrap domain.

    L-Glutamate → Human taste receptor TAS1R1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    T1R receptor molecular assays and computational model.
    limitations
    A supported binding model, not a directly observed ligand-bound structure in this paper.
    nutrient_topic
    Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
    plain_language
    Glutamate and its enhancer are not assigned the same binding site.
    primary_references
    Molecular mechanism for the umami taste synergism. · 2008 · https://pubmed.ncbi.nlm.nih.gov/19104071/ · DOI 10.1073/pnas.0810174106

    Monosodium Glutamate (MSG): taste, gut sensing, exposure and cross-nutrient mechanisms (2026-09-20) · lines 74–80

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · T1R receptor molecular assays and computational model. · source_derived_draft · unverified_draft

    ## monosodium-glutamate-umami-binding-model Glutamate and its enhancer are not assigned the same binding site. Receptor chimeras, mutagenesis and modeling support glutamate binding near the hinge of the T1R1 Venus-flytrap domain. Model: T1R receptor molecular assays and computational model. Limitations: A supported binding model, not a directly observed ligand-bound structure in this paper. Evidence access: Primary abstract Molecular mechanism for the umami taste synergism. · 2008 · https://pubmed.ncbi.nlm.nih.gov/19104071/ · DOI 10.1073/pnas.0810174106
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. 5-prime-ribonucleotides enhanced the human T1R1/T1R3 response to L-glutamate.

    Inosine 5-prime-monophosphate / IMP → Human umami receptor TAS1R1/TAS1R3 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human receptor coexpression and ligand-response assays.
    limitations
    A measured receptor interaction, not a general metabolic or clinical synergy.
    nutrient_topic
    L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
    plain_language
    A nucleotide can enhance the response to an amino acid at a receptor.
    primary_references
    Human receptors for sweet and umami taste. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11917125/ · DOI 10.1073/pnas.072090199

    L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19) · lines 50–56

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human receptor coexpression and ligand-response assays. · source_derived_draft · unverified_draft

    ## glutamate-umami-nucleotide A nucleotide can enhance the response to an amino acid at a receptor. 5-prime-ribonucleotides enhanced the human T1R1/T1R3 response to L-glutamate. Model: Human receptor coexpression and ligand-response assays. Limitations: A measured receptor interaction, not a general metabolic or clinical synergy. Evidence access: Primary abstract Human receptors for sweet and umami taste. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11917125/ · DOI 10.1073/pnas.072090199
    Complete structured claim and evidence

  2. Coexpressed human T1R1/T1R3 responded to L-glutamate in receptor assays.

    L-Glutamate → Human umami receptor TAS1R1/TAS1R3 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Heterologous expression of human taste receptors.
    limitations
    Taste-receptor activation does not establish a brain neurotransmitter effect.
    nutrient_topic
    L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
    plain_language
    Two receptor proteins recognize the umami signal.
    primary_references
    Human receptors for sweet and umami taste. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11917125/ · DOI 10.1073/pnas.072090199

    L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19) · lines 42–48

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Heterologous expression of human taste receptors. · source_derived_draft · unverified_draft

    ## glutamate-umami-receptor Two receptor proteins recognize the umami signal. Coexpressed human T1R1/T1R3 responded to L-glutamate in receptor assays. Model: Heterologous expression of human taste receptors. Limitations: Taste-receptor activation does not establish a brain neurotransmitter effect. Evidence access: Primary abstract Human receptors for sweet and umami taste. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11917125/ · DOI 10.1073/pnas.072090199
    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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