Component
DLAT knockdown in human colorectal cancer models
Study-specific entity. Experimental conditions and evidence limits remain on each linked claim.
3 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
DLAT knockdown reportedly increased ferroptosis susceptibility.
Experimental context and source evidence
- access_level
- abstract_only
- compartment
- Mitochondrial GSH versus intracellular GSH distinguished by authors
- dose
- Unknown: full methods unavailable
- duration
- Unknown: full methods unavailable
- endpoint
- ferroptosis
- evidence_location
- Primary indexed abstract; experiment-specific methods unavailable
- experimental_model
- Protein interaction/stability, knockdown and compound experiments reported in abstract
- exposure
- human-crc-dlat-knockdown
- limitations
- ABSTRACT-ONLY CURATION. Full article and supplements were not accessible; assay-specific cell line, dose, timing, controls and sample size remain unverified. No pulmonary-endothelial or clinical-treatment inference. The abstract does not identify each inducing exposure or rescue control.
- nutrient_topic
- Topical cross-reference only; no inheritance of another actor's effects. · GSH
- organism
- Human colorectal cancer models; individual experiments require full-text confirmation
- plain_language
- DLAT knockdown reportedly increased ferroptosis susceptibility.
- primary_locator
- [{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}]
- primary_references
- https://doi.org/10.1016/j.freeradbiomed.2026.04.133
- tissue_or_cell_type
- Colorectal cancer models; claim-specific cell line not established from abstract
DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 801–815
AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Protein interaction/stability, knockdown and compound experiments reported in abstract · source_derived_draft · unverified_draft
DLAT knockdown reportedly increased ferroptosis susceptibility. organism: Human colorectal cancer models; individual experiments require full-text confirmation tissue_or_cell_type: Colorectal cancer models; claim-specific cell line not established from abstract experimental_model: Protein interaction/stability, knockdown and compound experiments reported in abstract compartment: Mitochondrial GSH versus intracellular GSH distinguished by authors dose: Unknown: full methods unavailable duration: Unknown: full methods unavailable primary_references: https://doi.org/10.1016/j.freeradbiomed.2026.04.133 access_level: abstract_only evidence_location: Primary indexed abstract; experiment-specific methods unavailable endpoint: ferroptosis exposure: human-crc-dlat-knockdown limitations: ABSTRACT-ONLY CURATION. Full article and supplements were not accessible; assay-specific cell line, dose, timing, controls and sample size remain unverified. No pulmonary-endothelial or clinical-treatment inference. The abstract does not identify each inducing exposure or rescue control. primary_locator: [{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}] plain_language: DLAT knockdown reportedly increased ferroptosis susceptibility.
Complete structured claim and evidenceDLAT knockdown reportedly disrupted mitochondrial glutathione transport.
Experimental context and source evidence
- access_level
- abstract_only
- compartment
- Mitochondrial GSH versus intracellular GSH distinguished by authors
- dose
- Unknown: full methods unavailable
- duration
- Unknown: full methods unavailable
- endpoint
- mitochondrial-gsh-import
- evidence_location
- Primary indexed abstract; experiment-specific methods unavailable
- experimental_model
- Protein interaction/stability, knockdown and compound experiments reported in abstract
- exposure
- human-crc-dlat-knockdown
- limitations
- ABSTRACT-ONLY CURATION. Full article and supplements were not accessible; assay-specific cell line, dose, timing, controls and sample size remain unverified. No pulmonary-endothelial or clinical-treatment inference.
- nutrient_topic
- Topical cross-reference only; no inheritance of another actor's effects. · GSH
- organism
- Human colorectal cancer models; individual experiments require full-text confirmation
- plain_language
- DLAT knockdown reportedly disrupted mitochondrial glutathione transport.
- primary_locator
- [{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}]
- primary_references
- https://doi.org/10.1016/j.freeradbiomed.2026.04.133
- tissue_or_cell_type
- Colorectal cancer models; claim-specific cell line not established from abstract
DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 767–781
AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Protein interaction/stability, knockdown and compound experiments reported in abstract · source_derived_draft · unverified_draft
DLAT knockdown reportedly disrupted mitochondrial glutathione transport. organism: Human colorectal cancer models; individual experiments require full-text confirmation tissue_or_cell_type: Colorectal cancer models; claim-specific cell line not established from abstract experimental_model: Protein interaction/stability, knockdown and compound experiments reported in abstract compartment: Mitochondrial GSH versus intracellular GSH distinguished by authors dose: Unknown: full methods unavailable duration: Unknown: full methods unavailable primary_references: https://doi.org/10.1016/j.freeradbiomed.2026.04.133 access_level: abstract_only evidence_location: Primary indexed abstract; experiment-specific methods unavailable endpoint: mitochondrial-gsh-import exposure: human-crc-dlat-knockdown limitations: ABSTRACT-ONLY CURATION. Full article and supplements were not accessible; assay-specific cell line, dose, timing, controls and sample size remain unverified. No pulmonary-endothelial or clinical-treatment inference. primary_locator: [{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}] plain_language: DLAT knockdown reportedly disrupted mitochondrial glutathione transport.
Complete structured claim and evidenceDLAT knockdown reportedly increased lipid peroxidation.
Experimental context and source evidence
- access_level
- abstract_only
- compartment
- Mitochondrial GSH versus intracellular GSH distinguished by authors
- dose
- Unknown: full methods unavailable
- duration
- Unknown: full methods unavailable
- endpoint
- lipid-peroxidation
- evidence_location
- Primary indexed abstract; experiment-specific methods unavailable
- experimental_model
- Protein interaction/stability, knockdown and compound experiments reported in abstract
- exposure
- human-crc-dlat-knockdown
- limitations
- ABSTRACT-ONLY CURATION. Full article and supplements were not accessible; assay-specific cell line, dose, timing, controls and sample size remain unverified. No pulmonary-endothelial or clinical-treatment inference.
- nutrient_topic
- Topical cross-reference only; no inheritance of another actor's effects. · GSH
- organism
- Human colorectal cancer models; individual experiments require full-text confirmation
- plain_language
- DLAT knockdown reportedly increased lipid peroxidation.
- primary_locator
- [{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}]
- primary_references
- https://doi.org/10.1016/j.freeradbiomed.2026.04.133
- tissue_or_cell_type
- Colorectal cancer models; claim-specific cell line not established from abstract
DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 784–798
AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Protein interaction/stability, knockdown and compound experiments reported in abstract · source_derived_draft · unverified_draft
DLAT knockdown reportedly increased lipid peroxidation. organism: Human colorectal cancer models; individual experiments require full-text confirmation tissue_or_cell_type: Colorectal cancer models; claim-specific cell line not established from abstract experimental_model: Protein interaction/stability, knockdown and compound experiments reported in abstract compartment: Mitochondrial GSH versus intracellular GSH distinguished by authors dose: Unknown: full methods unavailable duration: Unknown: full methods unavailable primary_references: https://doi.org/10.1016/j.freeradbiomed.2026.04.133 access_level: abstract_only evidence_location: Primary indexed abstract; experiment-specific methods unavailable endpoint: lipid-peroxidation exposure: human-crc-dlat-knockdown limitations: ABSTRACT-ONLY CURATION. Full article and supplements were not accessible; assay-specific cell line, dose, timing, controls and sample size remain unverified. No pulmonary-endothelial or clinical-treatment inference. primary_locator: [{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}] plain_language: DLAT knockdown reportedly increased lipid peroxidation.
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.