Component

Human mitochondrial FPGS isoform

Human mitochondrial FPGS isoform; 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.

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.

Recorded relationships

What it acts on

  1. Mitochondrial-only FPGS expression relieved the glycine supplementation requirement of AUXB1 cells.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    experimental_model
    Human FPGS isoforms in Chinese hamster AUXB1 cells
    exposure
    Mitochondrial FPGS reconstitution with nutrient complementation
    limitations
    Growth complementation is indirect evidence of glycine synthetic capacity.
    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
    Restoring mitochondrial folate retention restored glycine independence.
    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 cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Folate and folic acid: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 315–325

    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-mito-glycine-complementation Mitochondrial-only FPGS expression relieved the glycine supplementation requirement of AUXB1 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: Restoring mitochondrial folate retention restored glycine independence. organism: Human enzyme in Cricetulus griseus cells tissue_or_cell_type: AUXB1 cells experimental_model: Human FPGS isoforms in Chinese hamster AUXB1 cells limitations: Growth complementation is indirect evidence of glycine synthetic capacity. exposure: Mitochondrial FPGS reconstitution with nutrient complementation [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
  2. Mitochondrial 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

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards