Human mitochondrial glutathione carrier SLC25A39

evidence_span

{"source_cache": "artifacts/glutathione-research/34707288.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7e6a64f24da95b93d7440f3424bb8a611f3fc962a5dd6344f5d0e11671e0bba5", "start_char": 0, "end_char": 1450, "text_sha256": "7e6a64f24da95b93d7440f3424bb8a611f3fc962a5dd6344f5d0e11671e0bba5"}

experimental_model

Organelle metabolomics, genetics and targeted synthesis rescue

exposure

SLC25A39 loss, A39/A40 double loss and targeted GshF

limitations

Mitochondrial versus total-cell pools differ; engineered synthesis rescue is not oral supplementation.

nutrient_topic

Glutathione research collection; topical membership is not evidence of a direct dietary effect. · GSH

organism

Mammalian cells; separate mouse erythropoiesis experiments

plain_language

Making glutathione is not enough if it cannot enter this compartment.

primary_references

[glutathione-p34707288] SLC25A39 is necessary for mitochondrial glutathione import in mammalian cells. (2021). https://pubmed.ncbi.nlm.nih.gov/34707288/ DOI: 10.1038/s41586-021-04025-w

tissue_or_cell_type

Mitochondria

Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 450–461

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Organelle metabolomics, genetics and targeted synthesis rescue · source_derived_draft · unverified_draft

### glutathione-a39-import SLC25A39 loss reduced mitochondrial GSH import. Condition category: normal nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: Making glutathione is not enough if it cannot enter this compartment. organism: Mammalian cells; separate mouse erythropoiesis experiments tissue_or_cell_type: Mitochondria experimental_model: Organelle metabolomics, genetics and targeted synthesis rescue limitations: Mitochondrial versus total-cell pools differ; engineered synthesis rescue is not oral supplementation. exposure: SLC25A39 loss, A39/A40 double loss and targeted GshF evidence_span: {"source_cache": "artifacts/glutathione-research/34707288.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7e6a64f24da95b93d7440f3424bb8a611f3fc962a5dd6344f5d0e11671e0bba5", "start_char": 0, "end_char": 1450, "text_sha256": "7e6a64f24da95b93d7440f3424bb8a611f3fc962a5dd6344f5d0e11671e0bba5"} [glutathione-p34707288] SLC25A39 is necessary for mitochondrial glutathione import in mammalian cells. (2021). https://pubmed.ncbi.nlm.nih.gov/34707288/ DOI: 10.1038/s41586-021-04025-w

evidence_span

{"source_cache": "artifacts/glutathione-research/35513392.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "000d49d8bad7e173d95c214f6cb2bf2ea84b9e4af231687687d1aa703cdeaff7", "start_char": 0, "end_char": 1457, "text_sha256": "000d49d8bad7e173d95c214f6cb2bf2ea84b9e4af231687687d1aa703cdeaff7"}

experimental_model

Paired CRISPR screen and mitochondrial transport assays

exposure

2016 single/pair perturbations across four metabolic states

limitations

Genetic buffering depends on metabolic conditions; it is not evidence that iron supplementation corrects low GSH.

nutrient_topic

Glutathione research collection; topical membership is not evidence of a direct dietary effect. · GSH

organism

Human experimental cells

plain_language

A second study supported the carrier assignment.

primary_references

[glutathione-p35513392] Combinatorial GxGxE CRISPR screen identifies SLC25A39 in mitochondrial glutathione transport linking iron homeostasis to OXPHOS. (2022). https://pubmed.ncbi.nlm.nih.gov/35513392/ DOI: 10.1038/s41467-022-30126-9

tissue_or_cell_type

Mitochondrial transport and respiration

Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 515–526

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Paired CRISPR screen and mitochondrial transport assays · source_derived_draft · unverified_draft

### glutathione-a39-independent An independent CRISPR/transport study identified SLC25A39 as critical for mitochondrial GSH import. Condition category: normal nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: A second study supported the carrier assignment. organism: Human experimental cells tissue_or_cell_type: Mitochondrial transport and respiration experimental_model: Paired CRISPR screen and mitochondrial transport assays limitations: Genetic buffering depends on metabolic conditions; it is not evidence that iron supplementation corrects low GSH. exposure: 2016 single/pair perturbations across four metabolic states evidence_span: {"source_cache": "artifacts/glutathione-research/35513392.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "000d49d8bad7e173d95c214f6cb2bf2ea84b9e4af231687687d1aa703cdeaff7", "start_char": 0, "end_char": 1457, "text_sha256": "000d49d8bad7e173d95c214f6cb2bf2ea84b9e4af231687687d1aa703cdeaff7"} [glutathione-p35513392] Combinatorial GxGxE CRISPR screen identifies SLC25A39 in mitochondrial glutathione transport linking iron homeostasis to OXPHOS. (2022). https://pubmed.ncbi.nlm.nih.gov/35513392/ DOI: 10.1038/s41467-022-30126-9

evidence_span

{"source_cache": "artifacts/glutathione-research/35513392.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "000d49d8bad7e173d95c214f6cb2bf2ea84b9e4af231687687d1aa703cdeaff7", "start_char": 0, "end_char": 1457, "text_sha256": "000d49d8bad7e173d95c214f6cb2bf2ea84b9e4af231687687d1aa703cdeaff7"}

experimental_model

Paired CRISPR screen and mitochondrial transport assays

exposure

2016 single/pair perturbations across four metabolic states

limitations

Genetic buffering depends on metabolic conditions; it is not evidence that iron supplementation corrects low GSH.

nutrient_topic

Glutathione research collection; topical membership is not evidence of a direct dietary effect. · GSH

organism

Human experimental cells

plain_language

Iron delivery and glutathione delivery met at mitochondrial energy production.

primary_references

[glutathione-p35513392] Combinatorial GxGxE CRISPR screen identifies SLC25A39 in mitochondrial glutathione transport linking iron homeostasis to OXPHOS. (2022). https://pubmed.ncbi.nlm.nih.gov/35513392/ DOI: 10.1038/s41467-022-30126-9

tissue_or_cell_type

Mitochondrial transport and respiration

Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 528–539

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Paired CRISPR screen and mitochondrial transport assays · source_derived_draft · unverified_draft

### glutathione-a39-iron-oxphos A39-mediated GSH homeostasis and A37-mediated iron uptake jointly supported OXPHOS in the genetic-interaction system. Condition category: normal nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: Iron delivery and glutathione delivery met at mitochondrial energy production. organism: Human experimental cells tissue_or_cell_type: Mitochondrial transport and respiration experimental_model: Paired CRISPR screen and mitochondrial transport assays limitations: Genetic buffering depends on metabolic conditions; it is not evidence that iron supplementation corrects low GSH. exposure: 2016 single/pair perturbations across four metabolic states evidence_span: {"source_cache": "artifacts/glutathione-research/35513392.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "000d49d8bad7e173d95c214f6cb2bf2ea84b9e4af231687687d1aa703cdeaff7", "start_char": 0, "end_char": 1457, "text_sha256": "000d49d8bad7e173d95c214f6cb2bf2ea84b9e4af231687687d1aa703cdeaff7"} [glutathione-p35513392] Combinatorial GxGxE CRISPR screen identifies SLC25A39 in mitochondrial glutathione transport linking iron homeostasis to OXPHOS. (2022). https://pubmed.ncbi.nlm.nih.gov/35513392/ DOI: 10.1038/s41467-022-30126-9

access_level

abstract_only

compartment

Mitochondrial GSH versus intracellular GSH distinguished by authors

dose

Unknown: full methods unavailable

duration

Unknown: full methods unavailable

endpoint

slc25a39

evidence_location

Primary indexed abstract; experiment-specific methods unavailable

experimental_model

Protein interaction/stability, knockdown and compound experiments reported in abstract

exposure

dlat

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

The abstract reports DLAT binding to SLC25A39 in colorectal cancer models.

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 716–730

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

The abstract reports DLAT binding to SLC25A39 in colorectal cancer models. 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: slc25a39 exposure: dlat 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: The abstract reports DLAT binding to SLC25A39 in colorectal cancer models.

evidence_span

{"source_cache": "artifacts/glutathione-research/38157846.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8910cd64daf32714af4c954a4781163c2c5be3270e58eba14f7ff481e8a2cc71", "start_char": 0, "end_char": 1145, "text_sha256": "8910cd64daf32714af4c954a4781163c2c5be3270e58eba14f7ff481e8a2cc71"}

experimental_model

Protein-interaction proteomics, knockout and neuronal regulation

exposure

AFG3L2 deletion and iron-sulfur sensing experiments

limitations

Protein-turnover regulation; no quantitative intake requirement is inferred.

nutrient_topic

Glutathione research collection; topical membership is not evidence of a direct dietary effect. · GSH

organism

Human carrier in mammalian systems

plain_language

The cell regulates carrier abundance by breaking down the protein.

primary_references

[glutathione-p38157846] Dual regulation of SLC25A39 by AFG3L2 and iron controls mitochondrial glutathione homeostasis. (2024). https://pubmed.ncbi.nlm.nih.gov/38157846/ DOI: 10.1016/j.molcel.2023.12.008

tissue_or_cell_type

Mitochondrial matrix-facing loop

Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 541–552

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Protein-interaction proteomics, knockout and neuronal regulation · source_derived_draft · unverified_draft

### glutathione-afg3l2-a39 AFG3L2 mediated SLC25A39 degradation through matrix loop 1. Condition category: normal nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cell regulates carrier abundance by breaking down the protein. organism: Human carrier in mammalian systems tissue_or_cell_type: Mitochondrial matrix-facing loop experimental_model: Protein-interaction proteomics, knockout and neuronal regulation limitations: Protein-turnover regulation; no quantitative intake requirement is inferred. exposure: AFG3L2 deletion and iron-sulfur sensing experiments evidence_span: {"source_cache": "artifacts/glutathione-research/38157846.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8910cd64daf32714af4c954a4781163c2c5be3270e58eba14f7ff481e8a2cc71", "start_char": 0, "end_char": 1145, "text_sha256": "8910cd64daf32714af4c954a4781163c2c5be3270e58eba14f7ff481e8a2cc71"} [glutathione-p38157846] Dual regulation of SLC25A39 by AFG3L2 and iron controls mitochondrial glutathione homeostasis. (2024). https://pubmed.ncbi.nlm.nih.gov/38157846/ DOI: 10.1016/j.molcel.2023.12.008

availability_state

machinery_impairment Imported condition classification; unverified.

experimental_model

Human K562 pooled CRISPR screen; two batches; paired SaCas9/SpCas9 guides

exposure

15-day growth screen; 25 mM glucose, 1 mM sodium pyruvate, 100 nM antimycin; 10% dialyzed FBS and 50 microgram/mL uridine.

limitations

Positive pi describes departure from an additive fitness expectation, not positive regulation between wild-type proteins. All four pi estimates are below the authors absolute pi >0.25 large-effect cutoff. Glucose significance value is below 0.02; other conditions are not. These are authors reported BH-adjusted values according to their archived pi_score code, not new p-values. Guide constructs are not independent biological replicates. No new genotype-by-environment significance test was performed.

organism

Human

primary_locator

Supplementary Data 3, Anti15_piscore and Anti15_pvalue, BD40 (row SLC25A39, column SLC16A11); Supplementary Data 4 All_Data_Sig_0.02 includes the glucose pair.

primary_references

https://doi.org/10.1038/s41467-022-30126-9

trigger_kind

machinery_impairment Imported condition classification; unverified.

SLC16A11 and mitochondrial glutathione: published screen connection and transport evidence · lines 24–30

Primary sources 2022 and 2017, plus labelled descriptive reanalysis on 2026-09-20. · supports · Human K562 pooled CRISPR screen; two batches; paired SaCas9/SpCas9 guides · source_derived_draft · unverified_draft

The published human K562 dual-targeting screen reports SLC16A11/SLC25A39 genetic interaction pi=0.0805858670811976 with significance value 0.612290402312043 under Anti15. This is a relative-fitness interaction estimate, not restoration of mitochondrial glutathione. primary_references: https://doi.org/10.1038/s41467-022-30126-9 primary_locator: Supplementary Data 3, Anti15_piscore and Anti15_pvalue, BD40 (row SLC25A39, column SLC16A11); Supplementary Data 4 All_Data_Sig_0.02 includes the glucose pair. organism: Human experimental_model: Human K562 pooled CRISPR screen; two batches; paired SaCas9/SpCas9 guides exposure: 15-day growth screen; 25 mM glucose, 1 mM sodium pyruvate, 100 nM antimycin; 10% dialyzed FBS and 50 microgram/mL uridine. limitations: Positive pi describes departure from an additive fitness expectation, not positive regulation between wild-type proteins. All four pi estimates are below the authors absolute pi >0.25 large-effect cutoff. Glucose significance value is below 0.02; other conditions are not. These are authors reported BH-adjusted values according to their archived pi_score code, not new p-values. Guide constructs are not independent biological replicates. No new genotype-by-environment significance test was performed.

availability_state

machinery_impairment Imported condition classification; unverified.

experimental_model

Human K562 pooled CRISPR screen; two batches; paired SaCas9/SpCas9 guides

exposure

15-day growth screen; 25 mM galactose replacing glucose, 1 mM sodium pyruvate; 10% dialyzed FBS and 50 microgram/mL uridine.

limitations

Positive pi describes departure from an additive fitness expectation, not positive regulation between wild-type proteins. All four pi estimates are below the authors absolute pi >0.25 large-effect cutoff. Glucose significance value is below 0.02; other conditions are not. These are authors reported BH-adjusted values according to their archived pi_score code, not new p-values. Guide constructs are not independent biological replicates. No new genotype-by-environment significance test was performed.

organism

Human

primary_locator

Supplementary Data 3, Gal15_piscore and Gal15_pvalue, BD40 (row SLC25A39, column SLC16A11); Supplementary Data 4 All_Data_Sig_0.02 includes the glucose pair.

primary_references

https://doi.org/10.1038/s41467-022-30126-9

trigger_kind

machinery_impairment Imported condition classification; unverified.

SLC16A11 and mitochondrial glutathione: published screen connection and transport evidence · lines 15–21

Primary sources 2022 and 2017, plus labelled descriptive reanalysis on 2026-09-20. · supports · Human K562 pooled CRISPR screen; two batches; paired SaCas9/SpCas9 guides · source_derived_draft · unverified_draft

The published human K562 dual-targeting screen reports SLC16A11/SLC25A39 genetic interaction pi=0.0272123713337914 with significance value 0.578178616323455 under Gal15. This is a relative-fitness interaction estimate, not restoration of mitochondrial glutathione. primary_references: https://doi.org/10.1038/s41467-022-30126-9 primary_locator: Supplementary Data 3, Gal15_piscore and Gal15_pvalue, BD40 (row SLC25A39, column SLC16A11); Supplementary Data 4 All_Data_Sig_0.02 includes the glucose pair. organism: Human experimental_model: Human K562 pooled CRISPR screen; two batches; paired SaCas9/SpCas9 guides exposure: 15-day growth screen; 25 mM galactose replacing glucose, 1 mM sodium pyruvate; 10% dialyzed FBS and 50 microgram/mL uridine. limitations: Positive pi describes departure from an additive fitness expectation, not positive regulation between wild-type proteins. All four pi estimates are below the authors absolute pi >0.25 large-effect cutoff. Glucose significance value is below 0.02; other conditions are not. These are authors reported BH-adjusted values according to their archived pi_score code, not new p-values. Guide constructs are not independent biological replicates. No new genotype-by-environment significance test was performed.

availability_state

machinery_impairment Imported condition classification; unverified.

experimental_model

Human K562 pooled CRISPR screen; two batches; paired SaCas9/SpCas9 guides

exposure

15-day growth screen; 25 mM glucose, 1 mM sodium pyruvate; 10% dialyzed FBS and 50 microgram/mL uridine.

limitations

Positive pi describes departure from an additive fitness expectation, not positive regulation between wild-type proteins. All four pi estimates are below the authors absolute pi >0.25 large-effect cutoff. Glucose significance value is below 0.02; other conditions are not. These are authors reported BH-adjusted values according to their archived pi_score code, not new p-values. Guide constructs are not independent biological replicates. No new genotype-by-environment significance test was performed.

organism

Human

primary_locator

Supplementary Data 3, Glc15_piscore and Glc15_pvalue, BD40 (row SLC25A39, column SLC16A11); Supplementary Data 4 All_Data_Sig_0.02 includes the glucose pair.

primary_references

https://doi.org/10.1038/s41467-022-30126-9

trigger_kind

machinery_impairment Imported condition classification; unverified.

SLC16A11 and mitochondrial glutathione: published screen connection and transport evidence · lines 6–12

Primary sources 2022 and 2017, plus labelled descriptive reanalysis on 2026-09-20. · supports · Human K562 pooled CRISPR screen; two batches; paired SaCas9/SpCas9 guides · source_derived_draft · unverified_draft

The published human K562 dual-targeting screen reports SLC16A11/SLC25A39 genetic interaction pi=0.154314615559463 with significance value 0.0185030434905457 under Glc15. This is a relative-fitness interaction estimate, not restoration of mitochondrial glutathione. primary_references: https://doi.org/10.1038/s41467-022-30126-9 primary_locator: Supplementary Data 3, Glc15_piscore and Glc15_pvalue, BD40 (row SLC25A39, column SLC16A11); Supplementary Data 4 All_Data_Sig_0.02 includes the glucose pair. organism: Human experimental_model: Human K562 pooled CRISPR screen; two batches; paired SaCas9/SpCas9 guides exposure: 15-day growth screen; 25 mM glucose, 1 mM sodium pyruvate; 10% dialyzed FBS and 50 microgram/mL uridine. limitations: Positive pi describes departure from an additive fitness expectation, not positive regulation between wild-type proteins. All four pi estimates are below the authors absolute pi >0.25 large-effect cutoff. Glucose significance value is below 0.02; other conditions are not. These are authors reported BH-adjusted values according to their archived pi_score code, not new p-values. Guide constructs are not independent biological replicates. No new genotype-by-environment significance test was performed.

availability_state

machinery_impairment Imported condition classification; unverified.

experimental_model

Human K562 pooled CRISPR screen; two batches; paired SaCas9/SpCas9 guides

exposure

15-day growth screen; 25 mM glucose, without added sodium pyruvate; 10% dialyzed FBS and 50 microgram/mL uridine.

limitations

Positive pi describes departure from an additive fitness expectation, not positive regulation between wild-type proteins. All four pi estimates are below the authors absolute pi >0.25 large-effect cutoff. Glucose significance value is below 0.02; other conditions are not. These are authors reported BH-adjusted values according to their archived pi_score code, not new p-values. Guide constructs are not independent biological replicates. No new genotype-by-environment significance test was performed.

organism

Human

primary_locator

Supplementary Data 3, Pyr15_piscore and Pyr15_pvalue, BD40 (row SLC25A39, column SLC16A11); Supplementary Data 4 All_Data_Sig_0.02 includes the glucose pair.

primary_references

https://doi.org/10.1038/s41467-022-30126-9

trigger_kind

machinery_impairment Imported condition classification; unverified.

SLC16A11 and mitochondrial glutathione: published screen connection and transport evidence · lines 33–39

Primary sources 2022 and 2017, plus labelled descriptive reanalysis on 2026-09-20. · supports · Human K562 pooled CRISPR screen; two batches; paired SaCas9/SpCas9 guides · source_derived_draft · unverified_draft

The published human K562 dual-targeting screen reports SLC16A11/SLC25A39 genetic interaction pi=0.155012680942449 with significance value 0.0621187730457448 under Pyr15. This is a relative-fitness interaction estimate, not restoration of mitochondrial glutathione. primary_references: https://doi.org/10.1038/s41467-022-30126-9 primary_locator: Supplementary Data 3, Pyr15_piscore and Pyr15_pvalue, BD40 (row SLC25A39, column SLC16A11); Supplementary Data 4 All_Data_Sig_0.02 includes the glucose pair. organism: Human experimental_model: Human K562 pooled CRISPR screen; two batches; paired SaCas9/SpCas9 guides exposure: 15-day growth screen; 25 mM glucose, without added sodium pyruvate; 10% dialyzed FBS and 50 microgram/mL uridine. limitations: Positive pi describes departure from an additive fitness expectation, not positive regulation between wild-type proteins. All four pi estimates are below the authors absolute pi >0.25 large-effect cutoff. Glucose significance value is below 0.02; other conditions are not. These are authors reported BH-adjusted values according to their archived pi_score code, not new p-values. Guide constructs are not independent biological replicates. No new genotype-by-environment significance test was performed.

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

dlat

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. Mechanistic interpretation reported in abstract; mediation/rescue controls cannot be assessed without full text.

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

The authors connect DLAT-associated transporter stabilization with maintained mitochondrial glutathione import.

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 750–764

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

The authors connect DLAT-associated transporter stabilization with maintained mitochondrial glutathione import. 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: dlat 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. Mechanistic interpretation reported in abstract; mediation/rescue controls cannot be assessed without full text. primary_locator: [{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}] plain_language: The authors connect DLAT-associated transporter stabilization with maintained mitochondrial glutathione import.

access_level

abstract_only

compartment

Mitochondrial GSH versus intracellular GSH distinguished by authors

dose

Unknown: full methods unavailable

duration

Unknown: full methods unavailable

endpoint

slc25a39-protein-stability

evidence_location

Primary indexed abstract; experiment-specific methods unavailable

experimental_model

Protein interaction/stability, knockdown and compound experiments reported in abstract

exposure

dlat

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 reportedly stabilized SLC25A39 independently of intracellular glutathione levels.

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 733–747

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 reportedly stabilized SLC25A39 independently of intracellular glutathione levels. 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: slc25a39-protein-stability exposure: dlat 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 reportedly stabilized SLC25A39 independently of intracellular glutathione levels.

evidence_span

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experimental_model

Protein-interaction proteomics, knockout and neuronal regulation

exposure

AFG3L2 deletion and iron-sulfur sensing experiments

limitations

Protein-turnover regulation; no quantitative intake requirement is inferred.

nutrient_topic

Glutathione research collection; topical membership is not evidence of a direct dietary effect. · GSH

organism

Human carrier in mammalian systems

plain_language

A cofactor-related signal changed how long the carrier persisted.

primary_references

[glutathione-p38157846] Dual regulation of SLC25A39 by AFG3L2 and iron controls mitochondrial glutathione homeostasis. (2024). https://pubmed.ncbi.nlm.nih.gov/38157846/ DOI: 10.1016/j.molcel.2023.12.008

tissue_or_cell_type

Mitochondrial matrix-facing loop

Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 554–565

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Protein-interaction proteomics, knockout and neuronal regulation · source_derived_draft · unverified_draft

### glutathione-a39-fes-stability Four matrix cysteines mediated iron-sulfur sensing that inhibited A39 degradation. Condition category: normal nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: A cofactor-related signal changed how long the carrier persisted. organism: Human carrier in mammalian systems tissue_or_cell_type: Mitochondrial matrix-facing loop experimental_model: Protein-interaction proteomics, knockout and neuronal regulation limitations: Protein-turnover regulation; no quantitative intake requirement is inferred. exposure: AFG3L2 deletion and iron-sulfur sensing experiments evidence_span: {"source_cache": "artifacts/glutathione-research/38157846.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8910cd64daf32714af4c954a4781163c2c5be3270e58eba14f7ff481e8a2cc71", "start_char": 0, "end_char": 1145, "text_sha256": "8910cd64daf32714af4c954a4781163c2c5be3270e58eba14f7ff481e8a2cc71"} [glutathione-p38157846] Dual regulation of SLC25A39 by AFG3L2 and iron controls mitochondrial glutathione homeostasis. (2024). https://pubmed.ncbi.nlm.nih.gov/38157846/ DOI: 10.1016/j.molcel.2023.12.008