Component
Jurkat T cell
Jurkat T cell. Species, exposure and limitations are retained in each linked claim.
1 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
Where it participates (unsigned role)
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.
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
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
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.