Component
Mouse ninjurin-1 / Ninj1
Context-specific entity; species, compartment and exposure are stated on each 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)
Glycine at 5 mM reduced LDH release in mouse macrophages undergoing tested pyroptotic, necrotic and post-apoptotic lysis, with no additional protection in Ninj1-knockout cells.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Mouse iBMDM knockout and glycine comparisons; stimulus-specific exposure durations.
- limitations
- No-additivity supports a shared process, not proof of direct glycine binding to NINJ1.
- nutrient_topic
- Glycine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Glycine
- plain_language
- A late membrane-rupture step was inhibited across several injury models.
- primary_references
- Glycine inhibits NINJ1 membrane clustering to suppress plasma membrane rupture in cell death. · 2022 · https://pubmed.ncbi.nlm.nih.gov/36468682/ · DOI 10.7554/eLife.78609
Glycine: supply, one-carbon allocation, receptors and cross-nutrient mechanisms (2026-09-19) · lines 354–360
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse iBMDM knockout and glycine comparisons; stimulus-specific exposure durations. · source_derived_draft · unverified_draft
## glycine-ninj1-mouse A late membrane-rupture step was inhibited across several injury models. Glycine at 5 mM reduced LDH release in mouse macrophages undergoing tested pyroptotic, necrotic and post-apoptotic lysis, with no additional protection in Ninj1-knockout cells. Model: Mouse iBMDM knockout and glycine comparisons; stimulus-specific exposure durations. Limitations: No-additivity supports a shared process, not proof of direct glycine binding to NINJ1. Evidence access: Primary full text Glycine inhibits NINJ1 membrane clustering to suppress plasma membrane rupture in cell death. · 2022 · https://pubmed.ncbi.nlm.nih.gov/36468682/ · DOI 10.7554/eLife.78609
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.