Component

Mouse p38 MAP kinase family, isoform unresolved

Mouse p38 MAP kinase family, isoform unresolved. Species, exposure and limitations are retained in each linked 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. Inhibition of p38 MAPK activity markedly attenuated cinnamaldehyde-induced thermogenic responses in mouse adipocytes.

    Mouse p38 MAP kinase family, isoform unresolved → Mouse adipocyte thermogenic gene program source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/ceylon-research/29046261.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0e0bba821363dc1d8ecdd40d3957b7d48778605b0d72bcf9016a26466cb2aac", "start_char": 0, "end_char": 1763, "text_sha256": "c0e0bba821363dc1d8ecdd40d3957b7d48778605b0d72bcf9016a26466cb2aac"}
    experimental_model
    Primary adipocyte signaling with inhibitor and knockout experiments
    exposure
    Acute and chronic purified cinnamaldehyde exposure
    limitations
    Cell thermogenesis is not a measured increase in whole-person energy expenditure or proven weight loss.
    nutrient_topic
    Ceylon cinnamon research collection; topical membership is not evidence of a direct dietary effect. · Ceylon cinnamon / Cinnamomum verum bark preparations
    organism
    Mouse; human donor-derived adipocytes
    plain_language
    Interfering with this signaling step weakened the cellular response.
    primary_references
    [ceylon-p29046261] Cinnamaldehyde induces fat cell-autonomous thermogenesis and metabolic reprogramming. (2017). https://pubmed.ncbi.nlm.nih.gov/29046261/ DOI: 10.1016/j.metabol.2017.08.006
    tissue_or_cell_type
    Subcutaneous adipocytes in culture
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Ceylon cinnamon: metabolism, signaling and nutrient connections (2026-09-17) · lines 584–595

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary adipocyte signaling with inhibitor and knockout experiments · source_derived_draft · unverified_draft

    ### ceylon-p38-block Inhibition of p38 MAPK activity markedly attenuated cinnamaldehyde-induced thermogenic responses in mouse adipocytes. Condition category: machinery_impairment nutrient_topic: Ceylon cinnamon research collection; topical membership is not evidence of a direct dietary effect. plain_language: Interfering with this signaling step weakened the cellular response. organism: Mouse; human donor-derived adipocytes tissue_or_cell_type: Subcutaneous adipocytes in culture experimental_model: Primary adipocyte signaling with inhibitor and knockout experiments limitations: Cell thermogenesis is not a measured increase in whole-person energy expenditure or proven weight loss. exposure: Acute and chronic purified cinnamaldehyde exposure evidence_span: {"source_cache": "artifacts/ceylon-research/29046261.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0e0bba821363dc1d8ecdd40d3957b7d48778605b0d72bcf9016a26466cb2aac", "start_char": 0, "end_char": 1763, "text_sha256": "c0e0bba821363dc1d8ecdd40d3957b7d48778605b0d72bcf9016a26466cb2aac"} [ceylon-p29046261] Cinnamaldehyde induces fat cell-autonomous thermogenesis and metabolic reprogramming. (2017). https://pubmed.ncbi.nlm.nih.gov/29046261/ DOI: 10.1016/j.metabol.2017.08.006
    Complete structured claim and evidence

What acts on it

  1. MAPK activation was repressed in the same stimulated macrophages.

    Nattokinase / subtilisin NAT → Mouse p38 MAP kinase family, isoform unresolved source_derived_draftungraded
    Experimental context and source evidence
    duration
    Not stated here
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    Mouse RAW264.7 macrophages
    exposure
    Nattokinase
    limitations
    The abstract names the family, not the isoform, so this is recorded against the mouse p38 family node the ledger already uses for isoform-unresolved reports.
    organism
    Mouse RAW264.7 macrophages
    plain_language
    MAPK activation was repressed in the same stimulated macrophages.
    primary_references
    Breaking the vicious loop between inflammation, oxidative stress and coagulation, a novel anti-thrombus insight of nattokinase by inhibiting LPS-induced inflammation and oxidative stress. (2020) https://pubmed.ncbi.nlm.nih.gov/32193146/ DOI: 10.1016/j.redox.2020.101500
    route
    In vitro
    tissue
    Cultured macrophages, LPS-stimulated

    Nattokinase: what the purified enzyme cleaves, what survives being eaten, and the gap between the two (2026-09-23) · lines 510–510

    Original AI-assisted curation built from a supplied entity-first document of 105 entities and 129 claims. Every reference in that document was resolved against live PubMed with its abstract read and its DOI cross-checked on 2026-09-23, and the EFSA novel-food opinion was retrieved and read in full. That check corrected two PMIDs that pointed at unrelated papers, two DOIs, and two papers recorded as carrying no erratum that do carry one; it also reversed three findings the supplied document had stated backwards. Two papers carry a published correction, recorded as such and not as a retraction. Three sources are not indexed in PubMed and are cited by what they have. Laboratory lineages are recorded, so the four papers from one group, the three from another and the two readings of a single applicant dossier cannot be counted as separate lines of support. Study-specific doses, units, populations and limitations retained; activity units are never converted between systems. Not publisher full text. · supports · Mouse RAW264.7 macrophages · source_derived_draft · unverified_draft

    MAPK activation was repressed in the same stimulated macrophages.
    Complete structured claim and evidence

  2. Nasunin attenuated p38 phosphorylation in stimulated RAW264 cells.

    Nasunin → Mouse p38 MAP kinase family, isoform unresolved source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/nasunin-research/28812425.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7a697b4eb979f1e6349bc79f4d2ed0d3994de51dfed777a71fb04740819eeabf", "start_char": 0, "end_char": 1094, "text_sha256": "7a697b4eb979f1e6349bc79f4d2ed0d3994de51dfed777a71fb04740819eeabf"}
    experimental_model
    LPS-stimulated macrophage experiments
    exposure
    Dose-dependent nasunin treatment; exact dose/time not reported in indexed abstract
    limitations
    These measurements do not prove direct binding to Akt, p38, NF-kappa-B or NOS2; reduced NOS2 expression is not direct enzyme inhibition. Response is LPS/cell-context dependent.
    nutrient_topic
    Nasunin research collection; topical membership is not evidence of a direct dietary effect. · Nasunin
    organism
    Mouse RAW264 macrophages
    plain_language
    A separate kinase response also decreased.
    primary_references
    [nasunin-p28812425] Nasunin inhibits the lipopolysaccharide-induced pro-inflammatory mediator production in RAW264 mouse macrophages by suppressing ROS-mediated activation of PI3 K/Akt/NF-κB and p38 signaling pathways. (2017). https://pubmed.ncbi.nlm.nih.gov/28812425/ DOI: 10.1080/09168451.2017.1362973
    tissue_or_cell_type
    Inflammatory mediator secretion and signaling

    Nasunin: identity, redox chemistry and nutrient connections (2026-09-17) · lines 289–300

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · LPS-stimulated macrophage experiments · source_derived_draft · unverified_draft

    ### nasunin-p38-macrophage Nasunin attenuated p38 phosphorylation in stimulated RAW264 cells. Condition category: normal nutrient_topic: Nasunin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A separate kinase response also decreased. organism: Mouse RAW264 macrophages tissue_or_cell_type: Inflammatory mediator secretion and signaling experimental_model: LPS-stimulated macrophage experiments limitations: These measurements do not prove direct binding to Akt, p38, NF-kappa-B or NOS2; reduced NOS2 expression is not direct enzyme inhibition. Response is LPS/cell-context dependent. exposure: Dose-dependent nasunin treatment; exact dose/time not reported in indexed abstract evidence_span: {"source_cache": "artifacts/nasunin-research/28812425.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7a697b4eb979f1e6349bc79f4d2ed0d3994de51dfed777a71fb04740819eeabf", "start_char": 0, "end_char": 1094, "text_sha256": "7a697b4eb979f1e6349bc79f4d2ed0d3994de51dfed777a71fb04740819eeabf"} [nasunin-p28812425] Nasunin inhibits the lipopolysaccharide-induced pro-inflammatory mediator production in RAW264 mouse macrophages by suppressing ROS-mediated activation of PI3 K/Akt/NF-κB and p38 signaling pathways. (2017). https://pubmed.ncbi.nlm.nih.gov/28812425/ DOI: 10.1080/09168451.2017.1362973
    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