Component

Human ninjurin-1 / NINJ1

Context-specific entity; species, compartment and exposure are stated on each 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 acts on it

  1. In primary human macrophages, 50 mM glycine inhibited pyroptosis-associated NINJ1 clustering and membrane rupture; NINJ1 knockdown produced a similar rupture phenotype.

    Glycine → Human ninjurin-1 / NINJ1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Human monocyte-derived macrophages, LPS/nigericin, native-protein analysis and knockdown.
    limitations
    Direct or indirect target engagement remains unresolved; 50 mM bath exposure is not a dietary plasma concentration.
    nutrient_topic
    Glycine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Glycine
    plain_language
    The membrane effect also occurred in human cells at a much higher experimental exposure.
    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 362–368

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human monocyte-derived macrophages, LPS/nigericin, native-protein analysis and knockdown. · source_derived_draft · unverified_draft

    ## glycine-ninj1-human-clustering The membrane effect also occurred in human cells at a much higher experimental exposure. In primary human macrophages, 50 mM glycine inhibited pyroptosis-associated NINJ1 clustering and membrane rupture; NINJ1 knockdown produced a similar rupture phenotype. Model: Human monocyte-derived macrophages, LPS/nigericin, native-protein analysis and knockdown. Limitations: Direct or indirect target engagement remains unresolved; 50 mM bath exposure is not a dietary plasma concentration. 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

Where it participates (unsigned role)

  1. Glycine did not protect primary human macrophages from the tested zVAD/BV6/TNF-induced necroptotic rupture.

    Glycine → Necroptotic rupture in human macrophages source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Primary human macrophages under a defined necroptosis protocol.
    limitations
    Different death execution pathways explain a context boundary; do not label this a conflicting replication of pyroptosis.
    nutrient_topic
    Glycine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Glycine
    plain_language
    The same protection did not apply to every route of cell death.
    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 378–384

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Primary human macrophages under a defined necroptosis protocol. · source_derived_draft · unverified_draft

    ## glycine-ninj1-necroptosis-limit The same protection did not apply to every route of cell death. Glycine did not protect primary human macrophages from the tested zVAD/BV6/TNF-induced necroptotic rupture. Model: Primary human macrophages under a defined necroptosis protocol. Limitations: Different death execution pathways explain a context boundary; do not label this a conflicting replication of pyroptosis. 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

  2. Human pyroptotic macrophages protected from rupture by glycine still lost mitochondrial membrane potential and ATP.

    Glycine → Energy viability in pyroptotic human macrophages source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Primary human macrophage energy/viability measurements alongside LDH assays.
    limitations
    The outcome is suppression of rupture, not reversal of upstream cell death.
    nutrient_topic
    Glycine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Glycine
    plain_language
    An intact membrane did not mean the cell survived.
    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 370–376

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Primary human macrophage energy/viability measurements alongside LDH assays. · source_derived_draft · unverified_draft

    ## glycine-ninj1-viability-limit An intact membrane did not mean the cell survived. Human pyroptotic macrophages protected from rupture by glycine still lost mitochondrial membrane potential and ATP. Model: Primary human macrophage energy/viability measurements alongside LDH assays. Limitations: The outcome is suppression of rupture, not reversal of upstream cell death. 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

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