Component

NFATC1

Independent biological entity. Read linked claims for experimental scope and context.

2 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

Where it participates (unsigned role)

  1. AM404 was a potent inhibitor of T-cell-receptor-mediated T-cell activation, specifically inhibiting interleukin-2 and tumour necrosis factor alpha gene transcription and tumour necrosis factor alpha synthesis in stimulated Jurkat T cells in a fatty acid amide hydrolase independent way, inhibiting both the binding to DNA and the transcriptional activity of endogenous nuclear factor of activated T cells without affecting early steps such as calcium mobilization or dephosphorylation, and without interfering with the pathways leading to AP-1 or nuclear factor kappa B activation.

    AM404 / N-arachidonoylphenolamine → Nuclear factor of activated T cells signalling source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/paracetamol-research/17196940.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "adb730eafbac5bf2eeb05418523f3f943b2b4f0ffb83e8e80cdc97c6f0ce27e9", "start_char": 0, "end_char": 1544, "text_sha256": "adb730eafbac5bf2eeb05418523f3f943b2b4f0ffb83e8e80cdc97c6f0ce27e9"}
    experimental_model
    Jurkat T cells stimulated through the T-cell receptor with transcription factor reporter assays
    exposure
    AM404 applied to CD3 and CD28-stimulated cells, with fatty acid amide hydrolase independence tested
    limitations
    Identifies a target of the metabolite that has nothing to do with pain. Cell line work at concentrations that are not related here to those reached in a person.
    nutrient_topic
    Paracetamol research collection; topical membership is not evidence of a direct clinical effect, and the drug is recorded separately from the metabolites NAPQI and AM404. · Paracetamol
    organism
    Human cells
    plain_language
    The metabolite also switches off a transcription factor that immune cells use, by a route unrelated to the enzyme that made it.
    primary_references
    [apap-p17196940] The acetaminophen-derived bioactive N-acylphenolamine AM404 inhibits NFAT by targeting nuclear regulatory events. (2007). https://pubmed.ncbi.nlm.nih.gov/17196940/ DOI: 10.1016/j.bcp.2006.12.001
    tissue_or_cell_type
    T lymphocytes

    Paracetamol: the enzyme it reduces rather than blocks, the isoform that turned out not to exist, the metabolite that carries the analgesia, and the metabolite that destroys the liver (2026-09-22) · lines 389–400

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Jurkat T cells stimulated through the T-cell receptor with transcription factor reporter assays · source_derived_draft · unverified_draft

    ### apap-am404-blocks-nfat AM404 was a potent inhibitor of T-cell-receptor-mediated T-cell activation, specifically inhibiting interleukin-2 and tumour necrosis factor alpha gene transcription and tumour necrosis factor alpha synthesis in stimulated Jurkat T cells in a fatty acid amide hydrolase independent way, inhibiting both the binding to DNA and the transcriptional activity of endogenous nuclear factor of activated T cells without affecting early steps such as calcium mobilization or dephosphorylation, and without interfering with the pathways leading to AP-1 or nuclear factor kappa B activation. Condition category: normal nutrient_topic: Paracetamol research collection; topical membership is not evidence of a direct clinical effect, and the drug is recorded separately from the metabolites NAPQI and AM404. plain_language: The metabolite also switches off a transcription factor that immune cells use, by a route unrelated to the enzyme that made it. organism: Human cells tissue_or_cell_type: T lymphocytes experimental_model: Jurkat T cells stimulated through the T-cell receptor with transcription factor reporter assays limitations: Identifies a target of the metabolite that has nothing to do with pain. Cell line work at concentrations that are not related here to those reached in a person. exposure: AM404 applied to CD3 and CD28-stimulated cells, with fatty acid amide hydrolase independence tested evidence_span: {"source_cache": "artifacts/paracetamol-research/17196940.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "adb730eafbac5bf2eeb05418523f3f943b2b4f0ffb83e8e80cdc97c6f0ce27e9", "start_char": 0, "end_char": 1544, "text_sha256": "adb730eafbac5bf2eeb05418523f3f943b2b4f0ffb83e8e80cdc97c6f0ce27e9"} [apap-p17196940] The acetaminophen-derived bioactive N-acylphenolamine AM404 inhibits NFAT by targeting nuclear regulatory events. (2007). https://pubmed.ncbi.nlm.nih.gov/17196940/ DOI: 10.1016/j.bcp.2006.12.001
    Complete structured claim and evidence

  2. Retinoic acid suppressed RANK and RANKL-driven osteoclast differentiation in progenitor cultures.

    All-trans-retinoic acid → Receptor activator of NF-kappa-B / TNFRSF11A / RANK source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Retinoid/bone-cell stage-dependent response.
    experimental_model
    Human and mouse osteoclast progenitors.
    limitations
    Does not negate whole-bone resorption results; cell stage and neighboring cells differ.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Homo sapiens; Mus musculus
    plain_language
    The response differs when the experiment starts with isolated precursor cells.
    primary_references
    [va-hu2010] Retinoic acid increases proliferation of human osteoclast progenitors and inhibits RANKL-stimulated osteoclast differentiation by suppressing RANK (2010). https://pubmed.ncbi.nlm.nih.gov/20949013/ DOI: 10.1371/journal.pone.0013305
    tissue_or_cell_type
    Osteoclast precursors

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1638–1648

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human and mouse osteoclast progenitors. · source_derived_draft · unverified_draft

    ### va-retinoic-acid-precursor-rank Retinoic acid suppressed RANK and RANKL-driven osteoclast differentiation in progenitor cultures. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: The response differs when the experiment starts with isolated precursor cells. organism: Homo sapiens; Mus musculus tissue_or_cell_type: Osteoclast precursors experimental_model: Human and mouse osteoclast progenitors. limitations: Does not negate whole-bone resorption results; cell stage and neighboring cells differ. cross_nutrient: Retinoid/bone-cell stage-dependent response. [va-hu2010] Retinoic acid increases proliferation of human osteoclast progenitors and inhibits RANKL-stimulated osteoclast differentiation by suppressing RANK (2010). https://pubmed.ncbi.nlm.nih.gov/20949013/ DOI: 10.1371/journal.pone.0013305
    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