Component

Human taste receptor TAS1R3

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

11 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. T1R3 siRNA attenuated aspartame-associated barrier and claudin-3 changes in Caco-2 cells.

    Human taste receptor TAS1R3 → Human Caco-2 permeability during aspartame exposure source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Human cell-line siRNA perturbation.
    limitations
    Supports functional involvement, not proof of direct binding to T1R3 alone.
    nutrient_topic
    Aspartame collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Aspartame
    plain_language
    Removing a signaling component reduced the response.
    primary_references
    Artificial Sweeteners Disrupt Tight Junctions and Barrier Function in the Intestinal Epithelium through Activation of the Sweet Taste Receptor, T1R3. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32580504/ · DOI 10.3390/nu12061862
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Aspartame: digestion, taste, metabolite dependencies and experimental signaling (2026-09-20) · lines 210–216

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

    ## aspartame-t1r3-knockdown Removing a signaling component reduced the response. T1R3 siRNA attenuated aspartame-associated barrier and claudin-3 changes in Caco-2 cells. Model: Human cell-line siRNA perturbation. Limitations: Supports functional involvement, not proof of direct binding to T1R3 alone. Evidence access: Primary full text Artificial Sweeteners Disrupt Tight Junctions and Barrier Function in the Intestinal Epithelium through Activation of the Sweet Taste Receptor, T1R3. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32580504/ · DOI 10.3390/nu12061862
    Complete structured claim and evidence

Where it participates (unsigned role)

  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

  3. Mutagenesis identified eleven T1R2 residues important for aspartame responses: S40, Y103, D142, S144, S165, S168, Y215, D278, E302, D307 and R383.

    Human taste receptor TAS1R2 → Aspartame source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human receptor mutants and homology models.
    limitations
    Loss of response can affect binding, folding or activation; not every residue is necessarily a direct contact.
    nutrient_topic
    Aspartame collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Aspartame
    plain_language
    Small changes in the sensor can alter recognition.
    primary_references
    Characterization of the Binding Site of Aspartame in the Human Sweet Taste Receptor. · 2015 · https://pubmed.ncbi.nlm.nih.gov/26377607/ · DOI 10.1093/chemse/bjv045

    Aspartame: digestion, taste, metabolite dependencies and experimental signaling (2026-09-20) · lines 170–176

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human receptor mutants and homology models. · source_derived_draft · unverified_draft

    ## aspartame-binding-residues Small changes in the sensor can alter recognition. Mutagenesis identified eleven T1R2 residues important for aspartame responses: S40, Y103, D142, S144, S165, S168, Y215, D278, E302, D307 and R383. Model: Human receptor mutants and homology models. Limitations: Loss of response can affect binding, folding or activation; not every residue is necessarily a direct contact. Evidence access: Primary abstract Characterization of the Binding Site of Aspartame in the Human Sweet Taste Receptor. · 2015 · https://pubmed.ncbi.nlm.nih.gov/26377607/ · DOI 10.1093/chemse/bjv045
    Complete structured claim and evidence

  4. The model proposed two pocket waters bridging aspartame carbonyls to D142 and L279.

    Aspartame → Human taste receptor TAS1R2 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Docking refined with functional mutagenesis.
    limitations
    Proposed molecular model, not a directly resolved bound-water structure.
    nutrient_topic
    Aspartame collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Aspartame
    plain_language
    Water-mediated contacts are a testable structural explanation.
    primary_references
    Characterization of the Binding Site of Aspartame in the Human Sweet Taste Receptor. · 2015 · https://pubmed.ncbi.nlm.nih.gov/26377607/ · DOI 10.1093/chemse/bjv045

    Aspartame: digestion, taste, metabolite dependencies and experimental signaling (2026-09-20) · lines 178–184

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Docking refined with functional mutagenesis. · source_derived_draft · unverified_draft

    ## aspartame-binding-water-model Water-mediated contacts are a testable structural explanation. The model proposed two pocket waters bridging aspartame carbonyls to D142 and L279. Model: Docking refined with functional mutagenesis. Limitations: Proposed molecular model, not a directly resolved bound-water structure. Evidence access: Primary abstract Characterization of the Binding Site of Aspartame in the Human Sweet Taste Receptor. · 2015 · https://pubmed.ncbi.nlm.nih.gov/26377607/ · DOI 10.1093/chemse/bjv045
    Complete structured claim and evidence

  5. Human T1R2/T1R3 responded to aspartame in heterologous receptor assays.

    Aspartame → Human sweet taste receptor TAS1R2/TAS1R3 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary article response panel and abstract
    experimental_model
    Human receptor coexpression, aspartame response panel.
    limitations
    Receptor activation is not a quantified human insulin response.
    nutrient_topic
    Aspartame collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Aspartame
    plain_language
    The intact sweetener has a receptor action before its metabolites are considered.
    primary_references
    Human receptors for sweet and umami taste. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11917125/ · DOI 10.1073/pnas.072090199

    Aspartame: digestion, taste, metabolite dependencies and experimental signaling (2026-09-20) · lines 162–168

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

    ## aspartame-human-sweet-receptor The intact sweetener has a receptor action before its metabolites are considered. Human T1R2/T1R3 responded to aspartame in heterologous receptor assays. Model: Human receptor coexpression, aspartame response panel. Limitations: Receptor activation is not a quantified human insulin response. Evidence access: Primary article response panel and 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

  6. Human T1R2 amino-terminal-domain mutants showed ligand-specific and shared requirements across chemically different sweeteners.

    Human taste receptor TAS1R2 → Aspartame source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Site-directed mutagenesis and docking.
    limitations
    A shared receptor is not proof that all sweeteners have interchangeable systemic effects.
    nutrient_topic
    Aspartame collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Aspartame
    plain_language
    Aspartame and other sweeteners need not perturb every receptor contact equally.
    primary_references
    Characterization of the modes of binding between human sweet taste receptor and low-molecular-weight sweet compounds. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22536376/ · DOI 10.1371/journal.pone.0035380

    Aspartame: digestion, taste, metabolite dependencies and experimental signaling (2026-09-20) · lines 186–192

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Site-directed mutagenesis and docking. · source_derived_draft · unverified_draft

    ## aspartame-ligand-specific-sites Aspartame and other sweeteners need not perturb every receptor contact equally. Human T1R2 amino-terminal-domain mutants showed ligand-specific and shared requirements across chemically different sweeteners. Model: Site-directed mutagenesis and docking. Limitations: A shared receptor is not proof that all sweeteners have interchangeable systemic effects. Evidence access: Primary abstract Characterization of the modes of binding between human sweet taste receptor and low-molecular-weight sweet compounds. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22536376/ · DOI 10.1371/journal.pone.0035380
    Complete structured claim and evidence

  7. 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

  8. 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

  9. 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

  10. Sucrose elicited a calcium response in cells coexpressing human TAS1R2 and TAS1R3, but not either subunit alone.

    Sucrose → Human sweet taste receptor TAS1R2/TAS1R3 source_derived_draftungraded
    Experimental context and source evidence
    dose
    300 mM sucrose with or without 1.25 mM lactisole
    duration
    Acute calcium response
    evidence_access
    Selected primary full-text sections inspected via indexed PMC page; local XML has abstract only.
    evidence_scope
    literature_reviewed; source-specific curation
    experimental_model
    Human TAS1R2/TAS1R3 coexpressed with engineered G-alpha15 in HEK-derived cells
    exposure_scope
    Human receptor in an expression system
    limitations
    Engineered coupling and high assay concentration do not measure human dietary absorption. Rat lactisole sensitivity differs. Selected full-text sections inspected; archived XML is abstract only.
    nutrient_topic
    Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
    organism
    Human TAS1R2/TAS1R3 coexpressed with engineered G-alpha15 in HEK-derived cells
    plain_language
    Sucrose elicited a calcium response in cells coexpressing human TAS1R2 and TAS1R3, but not either subunit alone.
    primary_references
    Human receptors for sweet and umami taste. (2002). https://pubmed.ncbi.nlm.nih.gov/11917125/ DOI: 10.1073/pnas.072090199
    route
    In vitro receptor stimulation
    tissue
    Recombinant sweet-receptor calcium-response assay

    Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 55–65

    Original AI-assisted source-specific sucrose curation with shared canonical claims retained by identity. Primary-study citations, negative findings, exposure details and limitations preserved. Not publisher full text. · supports · Human TAS1R2/TAS1R3 coexpressed with engineered G-alpha15 in HEK-derived cells · source_derived_draft · unverified_draft

    ## sucrose-sweet-receptor Sucrose elicited a calcium response in cells coexpressing human TAS1R2 and TAS1R3, but not either subunit alone. Model/species: Human TAS1R2/TAS1R3 coexpressed with engineered G-alpha15 in HEK-derived cells Tissue: Recombinant sweet-receptor calcium-response assay Exposure: 300 mM sucrose with or without 1.25 mM lactisole Route: In vitro receptor stimulation Duration: Acute calcium response Exposure scope: Human receptor in an expression system Limits: Engineered coupling and high assay concentration do not measure human dietary absorption. Rat lactisole sensitivity differs. Selected full-text sections inspected; archived XML is abstract only. Reference: Human receptors for sweet and umami taste. (2002). https://pubmed.ncbi.nlm.nih.gov/11917125/ DOI: 10.1073/pnas.072090199 Access: Selected primary full-text sections inspected via indexed PMC page; local XML has abstract only.
    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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