Component
Human GCLC Arg127Cys, Pro158Leu, His370Leu and Pro414Leu variants
Human GCLC Arg127Cys, Pro158Leu, His370Leu and Pro414Leu variants. Species, exposure and limitations are retained in each linked 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 it acts on
All four mutant GCLC transfectants had lower GSH than wild type in Gclc-null mouse fibroblasts; Pro414Leu was most impaired.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/glutathione-research/21657237.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d0ef7f04eacc64f48cee159ed630014f38163f2b848bf36b99c4d371786f55d7", "start_char": 0, "end_char": 1854, "text_sha256": "d0ef7f04eacc64f48cee159ed630014f38163f2b848bf36b99c4d371786f55d7"}
- experimental_model
- Human variants in recombinant assays, mouse fibroblasts and yeast complementation
- exposure
- Four clinical GCLC variants with or without GCLM
- limitations
- Expression-system rescue does not establish a clinical therapy; Pro158Leu retains near-wild-type isolated kinetics.
- nutrient_topic
- Glutathione research collection; topical membership is not evidence of a direct dietary effect. · GSH
- organism
- Human GCLC/GCLM; mouse and yeast hosts
- plain_language
- Supply can fail because the synthesis machinery is defective.
- primary_references
- [glutathione-p21657237] Enzymatic defects underlying hereditary glutamate cysteine ligase deficiency are mitigated by association of the catalytic and regulatory subunits. (2011). https://pubmed.ncbi.nlm.nih.gov/21657237/ DOI: 10.1021/bi200708w
- tissue_or_cell_type
- GCL activity and cellular GSH
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 385–396
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human variants in recombinant assays, mouse fibroblasts and yeast complementation · source_derived_draft · unverified_draft
### glutathione-gclc-mutant-gsh All four mutant GCLC transfectants had lower GSH than wild type in Gclc-null mouse fibroblasts; Pro414Leu was most impaired. Condition category: machinery_impairment nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: Supply can fail because the synthesis machinery is defective. organism: Human GCLC/GCLM; mouse and yeast hosts tissue_or_cell_type: GCL activity and cellular GSH experimental_model: Human variants in recombinant assays, mouse fibroblasts and yeast complementation limitations: Expression-system rescue does not establish a clinical therapy; Pro158Leu retains near-wild-type isolated kinetics. exposure: Four clinical GCLC variants with or without GCLM evidence_span: {"source_cache": "artifacts/glutathione-research/21657237.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d0ef7f04eacc64f48cee159ed630014f38163f2b848bf36b99c4d371786f55d7", "start_char": 0, "end_char": 1854, "text_sha256": "d0ef7f04eacc64f48cee159ed630014f38163f2b848bf36b99c4d371786f55d7"} [glutathione-p21657237] Enzymatic defects underlying hereditary glutamate cysteine ligase deficiency are mitigated by association of the catalytic and regulatory subunits. (2011). https://pubmed.ncbi.nlm.nih.gov/21657237/ DOI: 10.1021/bi200708w
Complete structured claim and evidence
Where it participates (unsigned role)
Adding GCLM largely rescued impaired activity of recombinant GCLC Arg127Cys, His370Leu and Pro414Leu.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/glutathione-research/21657237.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d0ef7f04eacc64f48cee159ed630014f38163f2b848bf36b99c4d371786f55d7", "start_char": 0, "end_char": 1854, "text_sha256": "d0ef7f04eacc64f48cee159ed630014f38163f2b848bf36b99c4d371786f55d7"}
- experimental_model
- Human variants in recombinant assays, mouse fibroblasts and yeast complementation
- exposure
- Four clinical GCLC variants with or without GCLM
- limitations
- Expression-system rescue does not establish a clinical therapy; Pro158Leu retains near-wild-type isolated kinetics.
- nutrient_topic
- Glutathione research collection; topical membership is not evidence of a direct dietary effect. · GSH
- organism
- Human GCLC/GCLM; mouse and yeast hosts
- plain_language
- The partner subunit changed how a damaged catalytic subunit performed.
- primary_references
- [glutathione-p21657237] Enzymatic defects underlying hereditary glutamate cysteine ligase deficiency are mitigated by association of the catalytic and regulatory subunits. (2011). https://pubmed.ncbi.nlm.nih.gov/21657237/ DOI: 10.1021/bi200708w
- tissue_or_cell_type
- GCL activity and cellular GSH
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 398–409
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human variants in recombinant assays, mouse fibroblasts and yeast complementation · source_derived_draft · unverified_draft
### glutathione-gclm-mutant-rescue Adding GCLM largely rescued impaired activity of recombinant GCLC Arg127Cys, His370Leu and Pro414Leu. Condition category: machinery_impairment nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: The partner subunit changed how a damaged catalytic subunit performed. organism: Human GCLC/GCLM; mouse and yeast hosts tissue_or_cell_type: GCL activity and cellular GSH experimental_model: Human variants in recombinant assays, mouse fibroblasts and yeast complementation limitations: Expression-system rescue does not establish a clinical therapy; Pro158Leu retains near-wild-type isolated kinetics. exposure: Four clinical GCLC variants with or without GCLM evidence_span: {"source_cache": "artifacts/glutathione-research/21657237.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d0ef7f04eacc64f48cee159ed630014f38163f2b848bf36b99c4d371786f55d7", "start_char": 0, "end_char": 1854, "text_sha256": "d0ef7f04eacc64f48cee159ed630014f38163f2b848bf36b99c4d371786f55d7"} [glutathione-p21657237] Enzymatic defects underlying hereditary glutamate cysteine ligase deficiency are mitigated by association of the catalytic and regulatory subunits. (2011). https://pubmed.ncbi.nlm.nih.gov/21657237/ DOI: 10.1021/bi200708w
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.