Component

Mouse Gpr142

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

3 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. Phenylalanine-associated glucose-tolerance improvement persisted in Gpr142-knockout mice, and its modest islet insulin response was not significantly different between knockout and wild-type mice.

    Mouse Gpr142 → Mouse glucose-tolerance response to phenylalanine source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse receptor-knockout whole-animal and islet experiments.
    limitations
    This differs from the study tryptophan result; it does not negate GPR142 signaling in a different cell model.
    nutrient_topic
    L-Phenylalanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Phenylalanine
    plain_language
    A receptor that responds in a dish may not be essential for the overall response.
    primary_references
    GPR142 Controls Tryptophan-Induced Insulin and Incretin Hormone Secretion to Improve Glucose Metabolism. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27322810/ · DOI 10.1371/journal.pone.0157298
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Phenylalanine: transport, protein synthesis, cofactor recycling and cross-nutrient mechanisms (2026-09-19) · lines 302–308

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse receptor-knockout whole-animal and islet experiments. · source_derived_draft · unverified_draft

    ## l-phenylalanine-gpr142-dispensability A receptor that responds in a dish may not be essential for the overall response. Phenylalanine-associated glucose-tolerance improvement persisted in Gpr142-knockout mice, and its modest islet insulin response was not significantly different between knockout and wild-type mice. Model: Mouse receptor-knockout whole-animal and islet experiments. Limitations: This differs from the study tryptophan result; it does not negate GPR142 signaling in a different cell model. Evidence access: Primary full text GPR142 Controls Tryptophan-Induced Insulin and Incretin Hormone Secretion to Improve Glucose Metabolism. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27322810/ · DOI 10.1371/journal.pone.0157298
    Complete structured claim and evidence

What acts on it

  1. In STC-1 enteroendocrine cells, phenylalanine stimulated a GPR142/Gq-linked calcium response contributing to GLP-1 release.

    L-Phenylalanine → Mouse Gpr142 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse STC-1 cells, live-cell signaling and pharmacologic experiments.
    limitations
    Exposure details beyond the accessed abstract are unresolved; this is not direct human gut evidence.
    nutrient_topic
    L-Phenylalanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Phenylalanine
    plain_language
    A gut-cell model used a receptor-to-calcium pathway to release a hormone.
    primary_references
    Identification of a regulatory pathway of L-phenylalanine-induced GLP-1 secretion in the enteroendocrine L cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/34953208/ · DOI 10.1016/j.bbrc.2021.12.043

    L-Phenylalanine: transport, protein synthesis, cofactor recycling and cross-nutrient mechanisms (2026-09-19) · lines 310–316

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse STC-1 cells, live-cell signaling and pharmacologic experiments. · source_derived_draft · unverified_draft

    ## l-phenylalanine-stc-gpr142 A gut-cell model used a receptor-to-calcium pathway to release a hormone. In STC-1 enteroendocrine cells, phenylalanine stimulated a GPR142/Gq-linked calcium response contributing to GLP-1 release. Model: Mouse STC-1 cells, live-cell signaling and pharmacologic experiments. Limitations: Exposure details beyond the accessed abstract are unresolved; this is not direct human gut evidence. Evidence access: Primary abstract Identification of a regulatory pathway of L-phenylalanine-induced GLP-1 secretion in the enteroendocrine L cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/34953208/ · DOI 10.1016/j.bbrc.2021.12.043
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Phenylalanine activated transfected human and mouse GPR142 IP1 signaling with EC50 values around 3.5 and 2.8 mM, respectively.

    L-Phenylalanine → Human GPR142 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Human or mouse receptor expressed in HEK293 cells.
    limitations
    Millimolar cell-assay potency does not prove that GPR142 mediates every whole-animal phenylalanine response.
    nutrient_topic
    L-Phenylalanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Phenylalanine
    plain_language
    A second amino-acid receptor can respond to phenylalanine.
    primary_references
    GPR142 Controls Tryptophan-Induced Insulin and Incretin Hormone Secretion to Improve Glucose Metabolism. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27322810/ · DOI 10.1371/journal.pone.0157298

    L-Phenylalanine: transport, protein synthesis, cofactor recycling and cross-nutrient mechanisms (2026-09-19) · lines 294–300

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human or mouse receptor expressed in HEK293 cells. · source_derived_draft · unverified_draft

    ## l-phenylalanine-gpr142-sensing A second amino-acid receptor can respond to phenylalanine. Phenylalanine activated transfected human and mouse GPR142 IP1 signaling with EC50 values around 3.5 and 2.8 mM, respectively. Model: Human or mouse receptor expressed in HEK293 cells. Limitations: Millimolar cell-assay potency does not prove that GPR142 mediates every whole-animal phenylalanine response. Evidence access: Primary full text GPR142 Controls Tryptophan-Induced Insulin and Incretin Hormone Secretion to Improve Glucose Metabolism. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27322810/ · DOI 10.1371/journal.pone.0157298
    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