Component
DELE1 knockout in human cultured cells
Study-specific role and exposure are specified on each linked 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.
What it acts on
DELE1 knockout suppressed iron-chelation-induced ATF4 activation.
Experimental context and source evidence
- access_level
- selected_indexed_full_text_passages
- evidence_cache
- artifacts/discovery-research/round2-sources/primary-mechanism-passages.json; SHA256 81c0207494f0b2a22fd0af0d70528a5114dfd74367dd99f967f4ada68c53e8c3
- experimental_model
- HEK293-derived knockout clones 24/51
- exposure
- 16 hours; DFP 1 mM in its arm; DFO concentration unresolved
- limitations
- Selected indexed primary full-text passages reviewed; supplements not independently inspected in this round. These records do not demonstrate iron-chelation rescue of SLC25A39 loss, clinical benefit, or transfer to pulmonary endothelium.
- organism
- Human cultured cells; mouse xenograft host only for colonization endpoint
- plain_language
- DELE1 knockout suppressed iron-chelation-induced ATF4 activation.
- primary_locator
- https://pmc.ncbi.nlm.nih.gov/articles/PMC10329284/ Figure 4H
- primary_references
- https://doi.org/10.1016/j.molcel.2023.05.031
DELE1 bridge: iron sensing and mitochondrial-glutathione-dependent stress signaling · lines 103–112
Targeted primary-literature curation; selected indexed full-text passages, 2026-09-20. · supports · HEK293-derived knockout clones 24/51 · source_derived_draft · unverified_draft
DELE1 knockout suppressed iron-chelation-induced ATF4 activation. primary_references: https://doi.org/10.1016/j.molcel.2023.05.031 primary_locator: https://pmc.ncbi.nlm.nih.gov/articles/PMC10329284/ Figure 4H evidence_cache: artifacts/discovery-research/round2-sources/primary-mechanism-passages.json; SHA256 81c0207494f0b2a22fd0af0d70528a5114dfd74367dd99f967f4ada68c53e8c3 access_level: selected_indexed_full_text_passages experimental_model: HEK293-derived knockout clones 24/51 organism: Human cultured cells; mouse xenograft host only for colonization endpoint exposure: 16 hours; DFP 1 mM in its arm; DFO concentration unresolved limitations: Selected indexed primary full-text passages reviewed; supplements not independently inspected in this round. These records do not demonstrate iron-chelation rescue of SLC25A39 loss, clinical benefit, or transfer to pulmonary endothelium. plain_language: DELE1 knockout suppressed iron-chelation-induced ATF4 activation.
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.