Component
Mitochondrial folate accumulation
Steady-state folate accumulation in the mitochondrial compartment.
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 acts on it
Human SLC25A32 cDNA restored mitochondrial folate accumulation and complemented glycine auxotrophy in CHO glyB cells, supporting the original folate-carrier interpretation.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- Historical vitamin B9 interpretation of a carrier now implicated in vitamin B2 cofactor supply.
- evidence_location
- Abstract; complementation and mitochondrial folate accumulation
- experimental_model
- Human placental cDNA complementation of CHO glyB cells
- exposure
- Retroviral human cDNA and subcloned cDNA expression.
- limitations
- Steady-state accumulation and growth rescue do not distinguish direct folate transport from indirect metabolic rescue.
- nutrient_topic
- Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
- organism
- Human cDNA in Cricetulus griseus cells
- plain_language
- Early rescue experiments linked this carrier to mitochondrial folate availability.
- primary_references
- [transport-slc25a32-2000] Retrovirally mediated complementation of the glyB phenotype. Cloning of a human gene encoding the carrier for entry of folates into mitochondria. (2000). https://pubmed.ncbi.nlm.nih.gov/10978331/ DOI: 10.1074/jbc.M005163200
- tissue_or_cell_type
- Cultured CHO glyB cells
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 530–542
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human placental cDNA complementation of CHO glyB cells · source_derived_draft · unverified_draft
### transport-slc25a32-historical-folate-rescue Human SLC25A32 cDNA restored mitochondrial folate accumulation and complemented glycine auxotrophy in CHO glyB cells, supporting the original folate-carrier interpretation. Condition category: machinery_impairment nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Early rescue experiments linked this carrier to mitochondrial folate availability. organism: Human cDNA in Cricetulus griseus cells tissue_or_cell_type: Cultured CHO glyB cells experimental_model: Human placental cDNA complementation of CHO glyB cells limitations: Steady-state accumulation and growth rescue do not distinguish direct folate transport from indirect metabolic rescue. exposure: Retroviral human cDNA and subcloned cDNA expression. cross_nutrient: Historical vitamin B9 interpretation of a carrier now implicated in vitamin B2 cofactor supply. evidence_location: Abstract; complementation and mitochondrial folate accumulation [transport-slc25a32-2000] Retrovirally mediated complementation of the glyB phenotype. Cloning of a human gene encoding the carrier for entry of folates into mitochondria. (2000). https://pubmed.ncbi.nlm.nih.gov/10978331/ DOI: 10.1074/jbc.M005163200
Complete structured claim and evidenceMitochondrial human FPGS maintained a separately retained mitochondrial folate-polyglutamate pool in reconstituted AUXB1 cells.
Experimental context and source evidence
- experimental_model
- Human FPGS isoforms in Chinese hamster AUXB1 cells
- exposure
- Induced mitochondrial FPGS and fractionation
- limitations
- Compartment separation is specific to the validated fractionation experiment.
- nutrient_topic
- Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. · Folate (vitamin B9)
- organism
- Human enzyme in Cricetulus griseus cells
- plain_language
- Mitochondria make and keep their own folate tails.
- primary_references
- [lawrence2014] Mammalian mitochondrial and cytosolic folylpolyglutamate synthetase maintain the subcellular compartmentalization of folates (2014). https://pubmed.ncbi.nlm.nih.gov/25164808/ DOI: 10.1074/jbc.m114.593244
- tissue_or_cell_type
- AUXB1 mitochondria
Folate and folic acid: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 291–301
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human FPGS isoforms in Chinese hamster AUXB1 cells · source_derived_draft · unverified_draft
### folate-fpgs-mitochondrial-trapping Mitochondrial human FPGS maintained a separately retained mitochondrial folate-polyglutamate pool in reconstituted AUXB1 cells. Condition category: normal nutrient_topic: Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: Mitochondria make and keep their own folate tails. organism: Human enzyme in Cricetulus griseus cells tissue_or_cell_type: AUXB1 mitochondria experimental_model: Human FPGS isoforms in Chinese hamster AUXB1 cells limitations: Compartment separation is specific to the validated fractionation experiment. exposure: Induced mitochondrial FPGS and fractionation [lawrence2014] Mammalian mitochondrial and cytosolic folylpolyglutamate synthetase maintain the subcellular compartmentalization of folates (2014). https://pubmed.ncbi.nlm.nih.gov/25164808/ DOI: 10.1074/jbc.m114.593244
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.