Component
Iron–sulfur cluster assembly in isolated mouse-cell mitochondria
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 acts on it
Sulfur-35 cysteine supplied sulfur for newly assembled iron–sulfur clusters incorporated into aconitase and ferredoxins in isolated mouse neuronal-cell mitochondria.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mitochondria from mouse Cath.A-derived neuronal cells; radioactive sulfur tracing.
- limitations
- An isolated-organelle assembly assay is not evidence that more dietary cysteine corrects an iron–sulfur disease.
- nutrient_topic
- L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
- plain_language
- Cysteine supplies the sulfur half of an iron–sulfur cofactor.
- primary_references
- Fe-S cluster biogenesis in isolated mammalian mitochondria: coordinated use of persulfide sulfur and iron and requirements for GTP, NADH, and ATP. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25398879/ · DOI 10.1074/jbc.M114.610402
L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 268–274
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mitochondria from mouse Cath.A-derived neuronal cells; radioactive sulfur tracing. · source_derived_draft · unverified_draft
## l-cysteine-fe-s-sulfur-donor Cysteine supplies the sulfur half of an iron–sulfur cofactor. Sulfur-35 cysteine supplied sulfur for newly assembled iron–sulfur clusters incorporated into aconitase and ferredoxins in isolated mouse neuronal-cell mitochondria. Model: Mitochondria from mouse Cath.A-derived neuronal cells; radioactive sulfur tracing. Limitations: An isolated-organelle assembly assay is not evidence that more dietary cysteine corrects an iron–sulfur disease. Evidence access: Primary abstract Fe-S cluster biogenesis in isolated mammalian mitochondria: coordinated use of persulfide sulfur and iron and requirements for GTP, NADH, and ATP. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25398879/ · DOI 10.1074/jbc.M114.610402
Complete structured claim and evidenceLabeled NFS1-bound persulfide was an intermediate; its sulfur release required iron, GTP and NADH, whereas ATP was required for the overall assembly pathway but not this release step.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse-cell isolated mitochondrial experiments.
- limitations
- The proposed GTPase/reductase mediators were not individually established by this study; do not assign a universal ATP requirement to each substep.
- nutrient_topic
- L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
- plain_language
- The pathway has several gates, with different requirements at different steps.
- primary_references
- Fe-S cluster biogenesis in isolated mammalian mitochondria: coordinated use of persulfide sulfur and iron and requirements for GTP, NADH, and ATP. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25398879/ · DOI 10.1074/jbc.M114.610402
L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 276–282
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse-cell isolated mitochondrial experiments. · source_derived_draft · unverified_draft
## l-cysteine-nfs1-persulfide-gate The pathway has several gates, with different requirements at different steps. Labeled NFS1-bound persulfide was an intermediate; its sulfur release required iron, GTP and NADH, whereas ATP was required for the overall assembly pathway but not this release step. Model: Mouse-cell isolated mitochondrial experiments. Limitations: The proposed GTPase/reductase mediators were not individually established by this study; do not assign a universal ATP requirement to each substep. Evidence access: Primary abstract Fe-S cluster biogenesis in isolated mammalian mitochondria: coordinated use of persulfide sulfur and iron and requirements for GTP, NADH, and ATP. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25398879/ · DOI 10.1074/jbc.M114.610402
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.