Component

Disulfide stress in SLC7A11-high human cells

Context-specific entity; species, compartment and exposure are stated on each claim.

4 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. Glucose starvation of SLC7A11-high human cancer cells induced abnormal disulfide bonding in actin-cytoskeleton proteins, F-actin collapse and disulfidptosis, distinct from apoptosis and ferroptosis.

    Disulfide stress in SLC7A11-high human cells → Actin-cytoskeleton disulfide bonding and collapse in human cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary abstract and primary publisher figure descriptions
    experimental_model
    Human cancer cultures, chemical proteomics and cell-biological assays.
    limitations
    Experimental deprivation; do not infer this occurs whenever blood glucose falls modestly.
    nutrient_topic
    L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
    plain_language
    The damage involved cross-linked structural proteins rather than the same lipid-peroxide pathway.
    primary_references
    Actin cytoskeleton vulnerability to disulfide stress mediates disulfidptosis. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36747082/ · DOI 10.1038/s41556-023-01091-2
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 252–258

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human cancer cultures, chemical proteomics and cell-biological assays. · source_derived_draft · unverified_draft

    ## l-cysteine-disulfidptosis-actin The damage involved cross-linked structural proteins rather than the same lipid-peroxide pathway. Glucose starvation of SLC7A11-high human cancer cells induced abnormal disulfide bonding in actin-cytoskeleton proteins, F-actin collapse and disulfidptosis, distinct from apoptosis and ferroptosis. Model: Human cancer cultures, chemical proteomics and cell-biological assays. Limitations: Experimental deprivation; do not infer this occurs whenever blood glucose falls modestly. Evidence access: Primary abstract and primary publisher figure descriptions Actin cytoskeleton vulnerability to disulfide stress mediates disulfidptosis. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36747082/ · DOI 10.1038/s41556-023-01091-2
    Complete structured claim and evidence

What acts on it

  1. High SLC7A11-mediated cystine uptake increased reliance on glucose and the pentose phosphate pathway; glucose deprivation depleted NADPH and promoted intracellular disulfide accumulation.

    SLC7A11 → Disulfide stress in SLC7A11-high human cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Human cancer-cell transporter manipulation, glucose withdrawal and metabolic assays.
    limitations
    Complete glucose withdrawal in culture is not ordinary fasting or dietary carbohydrate restriction.
    nutrient_topic
    L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
    plain_language
    Importing more oxidized nutrient also creates more work for the reducing system.
    primary_references
    Cystine transporter regulation of pentose phosphate pathway dependency and disulfide stress exposes a targetable metabolic vulnerability in cancer. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32231310/ · DOI 10.1038/s41556-020-0496-x
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 236–242

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human cancer-cell transporter manipulation, glucose withdrawal and metabolic assays. · source_derived_draft · unverified_draft

    ## l-cysteine-cystine-nadph-demand Importing more oxidized nutrient also creates more work for the reducing system. High SLC7A11-mediated cystine uptake increased reliance on glucose and the pentose phosphate pathway; glucose deprivation depleted NADPH and promoted intracellular disulfide accumulation. Model: Human cancer-cell transporter manipulation, glucose withdrawal and metabolic assays. Limitations: Complete glucose withdrawal in culture is not ordinary fasting or dietary carbohydrate restriction. Evidence access: Primary full text Cystine transporter regulation of pentose phosphate pathway dependency and disulfide stress exposes a targetable metabolic vulnerability in cancer. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32231310/ · DOI 10.1038/s41556-020-0496-x
    Complete structured claim and evidence

  2. Preventing cystine uptake or removing cystine relieved the disulfide stress associated with glucose deprivation in SLC7A11-high cells.

    Cystine removal during glucose starvation → Disulfide stress in SLC7A11-high human cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Human cancer-cell glucose/cystine manipulation.
    limitations
    This is distinct from cystine-withdrawal ferroptosis under other conditions; no universal benefit of removing cystine is implied.
    nutrient_topic
    L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
    plain_language
    Reducing the incoming load helped when the cell could not process it.
    primary_references
    Cystine transporter regulation of pentose phosphate pathway dependency and disulfide stress exposes a targetable metabolic vulnerability in cancer. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32231310/ · DOI 10.1038/s41556-020-0496-x
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 244–250

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human cancer-cell glucose/cystine manipulation. · source_derived_draft · unverified_draft

    ## l-cysteine-cystine-reduction-rescue Reducing the incoming load helped when the cell could not process it. Preventing cystine uptake or removing cystine relieved the disulfide stress associated with glucose deprivation in SLC7A11-high cells. Model: Human cancer-cell glucose/cystine manipulation. Limitations: This is distinct from cystine-withdrawal ferroptosis under other conditions; no universal benefit of removing cystine is implied. Evidence access: Primary full text Cystine transporter regulation of pentose phosphate pathway dependency and disulfide stress exposes a targetable metabolic vulnerability in cancer. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32231310/ · DOI 10.1038/s41556-020-0496-x
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Inactivation of the WAVE regulatory complex suppressed disulfidptosis, whereas constitutive Rac activation promoted it in the studied cells.

    Human WAVE regulatory complex → Actin-cytoskeleton disulfide bonding and collapse in human cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Human cancer-cell CRISPR screens and functional perturbations.
    limitations
    A complex-level finding is not assigned to every WAVE subunit or Rac isoform without resolution.
    nutrient_topic
    L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
    plain_language
    The state of the actin-assembly machinery changed vulnerability to sulfur stress.
    primary_references
    Actin cytoskeleton vulnerability to disulfide stress mediates disulfidptosis. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36747082/ · DOI 10.1038/s41556-023-01091-2
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 260–266

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human cancer-cell CRISPR screens and functional perturbations. · source_derived_draft · unverified_draft

    ## l-cysteine-disulfidptosis-wave The state of the actin-assembly machinery changed vulnerability to sulfur stress. Inactivation of the WAVE regulatory complex suppressed disulfidptosis, whereas constitutive Rac activation promoted it in the studied cells. Model: Human cancer-cell CRISPR screens and functional perturbations. Limitations: A complex-level finding is not assigned to every WAVE subunit or Rac isoform without resolution. Evidence access: Primary abstract Actin cytoskeleton vulnerability to disulfide stress mediates disulfidptosis. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36747082/ · DOI 10.1038/s41556-023-01091-2
    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