Component
Human gamma-glutamyl hydrolase / GGH
Human gamma-glutamyl hydrolase / GGH; species and subcellular isoforms retained separately.
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.
Where it participates (unsigned role)
GGH overexpression lowered long-chain folate-polyglutamate content in HCT116 cells.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- experimental_model
- GGH-modulated human HCT116 cancer cells
- exposure
- Sense-GGH vector versus control
- limitations
- Long-chain content was estimated using conjugase-treated versus untreated assay differences.
- nutrient_topic
- Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. · Folate (vitamin B9)
- organism
- Homo sapiens
- plain_language
- More tail trimming reduced retained long-chain folates.
- primary_references
- [kim2013] γ-Glutamyl hydrolase modulation and folate influence chemosensitivity of cancer cells to 5-fluorouracil and methotrexate (2013). https://pubmed.ncbi.nlm.nih.gov/24045662/ DOI: 10.1038/bjc.2013.579
- tissue_or_cell_type
- HCT116 cells
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Folate and folic acid: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 327–337
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · GGH-modulated human HCT116 cancer cells · source_derived_draft · unverified_draft
### folate-ggh-overexpression-tail-loss GGH overexpression lowered long-chain folate-polyglutamate content in HCT116 cells. Condition category: machinery_impairment nutrient_topic: Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: More tail trimming reduced retained long-chain folates. organism: Homo sapiens tissue_or_cell_type: HCT116 cells experimental_model: GGH-modulated human HCT116 cancer cells limitations: Long-chain content was estimated using conjugase-treated versus untreated assay differences. exposure: Sense-GGH vector versus control [kim2013] γ-Glutamyl hydrolase modulation and folate influence chemosensitivity of cancer cells to 5-fluorouracil and methotrexate (2013). https://pubmed.ncbi.nlm.nih.gov/24045662/ DOI: 10.1038/bjc.2013.579
Complete structured claim and evidenceGGH-targeted siRNA increased long-chain folate-polyglutamate content in HCT116 cells.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- experimental_model
- GGH-modulated human HCT116 cancer cells
- exposure
- Targeted siRNA versus control
- limitations
- Does not imply universal drug sensitization across folate conditions.
- nutrient_topic
- Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. · Folate (vitamin B9)
- organism
- Homo sapiens
- plain_language
- Less tail trimming increased the retained folate pool.
- primary_references
- [kim2013] γ-Glutamyl hydrolase modulation and folate influence chemosensitivity of cancer cells to 5-fluorouracil and methotrexate (2013). https://pubmed.ncbi.nlm.nih.gov/24045662/ DOI: 10.1038/bjc.2013.579
- tissue_or_cell_type
- HCT116 cells
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Folate and folic acid: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 339–349
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · GGH-modulated human HCT116 cancer cells · source_derived_draft · unverified_draft
### folate-ggh-silencing-tail-retention GGH-targeted siRNA increased long-chain folate-polyglutamate content in HCT116 cells. Condition category: machinery_impairment nutrient_topic: Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: Less tail trimming increased the retained folate pool. organism: Homo sapiens tissue_or_cell_type: HCT116 cells experimental_model: GGH-modulated human HCT116 cancer cells limitations: Does not imply universal drug sensitization across folate conditions. exposure: Targeted siRNA versus control [kim2013] γ-Glutamyl hydrolase modulation and folate influence chemosensitivity of cancer cells to 5-fluorouracil and methotrexate (2013). https://pubmed.ncbi.nlm.nih.gov/24045662/ DOI: 10.1038/bjc.2013.579
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.