Component
p38-gamma assay protein in the 2018 ImP study; species unresolved in accessed abstract
Context-specific entity; species, compartment and exposure are stated on each claim.
2 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.
What it acts on
The 2018 study linked imidazole-propionate-activated p38-gamma to p62 phosphorylation.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Biochemical/cellular experiments summarized in the primary abstract; study also contains mouse intervention and human observations.
- limitations
- The abstract does not resolve species and construct for each biochemical step; assay proteins are not silently assigned human identity.
- nutrient_topic
- L-Histidine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Histidine
- plain_language
- A kinase relays the microbial-metabolite signal to an adaptor protein.
- primary_references
- Microbially Produced Imidazole Propionate Impairs Insulin Signaling through mTORC1. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30401435/ · DOI 10.1016/j.cell.2018.09.055
L-Histidine: supply, catabolism, histamine, receptors and cross-nutrient mechanisms (2026-09-19) · lines 306–312
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Biochemical/cellular experiments summarized in the primary abstract; study also contains mouse intervention and human observations. · source_derived_draft · unverified_draft
## histidine-imp-p38-p62 A kinase relays the microbial-metabolite signal to an adaptor protein. The 2018 study linked imidazole-propionate-activated p38-gamma to p62 phosphorylation. Model: Biochemical/cellular experiments summarized in the primary abstract; study also contains mouse intervention and human observations. Limitations: The abstract does not resolve species and construct for each biochemical step; assay proteins are not silently assigned human identity. Evidence access: Primary abstract Microbially Produced Imidazole Propionate Impairs Insulin Signaling through mTORC1. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30401435/ · DOI 10.1016/j.cell.2018.09.055
Complete structured claim and evidence
Where it participates (unsigned role)
The study connected p62 phosphorylation to mTORC1 activation and impaired signaling at insulin receptor substrate.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Primary abstract-level biochemical/cellular pathway report.
- limitations
- Complete construct, dose and cell-specific mapping remains a follow-up; this route is distinct from ordinary dietary histidine intake.
- nutrient_topic
- L-Histidine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Histidine
- plain_language
- The adaptor connects this branch to nutrient-sensitive signaling and insulin response.
- primary_references
- Microbially Produced Imidazole Propionate Impairs Insulin Signaling through mTORC1. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30401435/ · DOI 10.1016/j.cell.2018.09.055
L-Histidine: supply, catabolism, histamine, receptors and cross-nutrient mechanisms (2026-09-19) · lines 314–320
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Primary abstract-level biochemical/cellular pathway report. · source_derived_draft · unverified_draft
## histidine-imp-p62-mtor The adaptor connects this branch to nutrient-sensitive signaling and insulin response. The study connected p62 phosphorylation to mTORC1 activation and impaired signaling at insulin receptor substrate. Model: Primary abstract-level biochemical/cellular pathway report. Limitations: Complete construct, dose and cell-specific mapping remains a follow-up; this route is distinct from ordinary dietary histidine intake. Evidence access: Primary abstract Microbially Produced Imidazole Propionate Impairs Insulin Signaling through mTORC1. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30401435/ · DOI 10.1016/j.cell.2018.09.055
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.