Component

Human ALDH1L1

Homo sapiens protein; gene perturbations are separate gene entities.

2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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. Ectopic ALDH1L1 expression in HuH-7 cells increased ZMP/AICAR ribotide, consistent with reduced formyl-donor availability for ATIC.

    Human ALDH1L1 → 5-Aminoimidazole-4-carboxamide ribonucleotide source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Stable expression and metabolomics
    exposure
    Engineered ALDH1L1 expression.
    limitations
    Overexpression in one cancer line; substrate competition is the study interpretation.
    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
    Disposing of folate-bound carbon can slow a purine-building step.
    primary_references
    [sasaki-2023] One-carbon metabolizing enzyme ALDH1L1 influences mitochondrial metabolism through 5-aminoimidazole-4-carboxamide ribonucleotide accumulation and serine depletion, contributing to tumor suppression (2023). https://pubmed.ncbi.nlm.nih.gov/37596270/ DOI: 10.1038/s41598-023-38142-5
    tissue_or_cell_type
    HuH-7 hepatocellular carcinoma cells

    Folate and folic acid: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1072–1082

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Stable expression and metabolomics · source_derived_draft · unverified_draft

    ### aldh1l1-aicar-accumulation Ectopic ALDH1L1 expression in HuH-7 cells increased ZMP/AICAR ribotide, consistent with reduced formyl-donor availability for ATIC. Condition category: normal nutrient_topic: Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: Disposing of folate-bound carbon can slow a purine-building step. organism: Homo sapiens tissue_or_cell_type: HuH-7 hepatocellular carcinoma cells experimental_model: Stable expression and metabolomics limitations: Overexpression in one cancer line; substrate competition is the study interpretation. exposure: Engineered ALDH1L1 expression. [sasaki-2023] One-carbon metabolizing enzyme ALDH1L1 influences mitochondrial metabolism through 5-aminoimidazole-4-carboxamide ribonucleotide accumulation and serine depletion, contributing to tumor suppression (2023). https://pubmed.ncbi.nlm.nih.gov/37596270/ DOI: 10.1038/s41598-023-38142-5
    Complete structured claim and evidence

  2. ALDH1L1-expressing HuH-7 cells had lower serine and higher glycine than controls.

    Human ALDH1L1 → L-Serine source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Cell metabolomics
    exposure
    Engineered ALDH1L1 expression.
    limitations
    Pool changes alone do not quantify compartment-specific SHMT flux.
    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
    Changing folate-carbon disposal reshaped amino-acid pools.
    primary_references
    [sasaki-2023] One-carbon metabolizing enzyme ALDH1L1 influences mitochondrial metabolism through 5-aminoimidazole-4-carboxamide ribonucleotide accumulation and serine depletion, contributing to tumor suppression (2023). https://pubmed.ncbi.nlm.nih.gov/37596270/ DOI: 10.1038/s41598-023-38142-5
    tissue_or_cell_type
    HuH-7 cells

    Folate and folic acid: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1084–1094

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell metabolomics · source_derived_draft · unverified_draft

    ### aldh1l1-serine-glycine ALDH1L1-expressing HuH-7 cells had lower serine and higher glycine than controls. Condition category: normal nutrient_topic: Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: Changing folate-carbon disposal reshaped amino-acid pools. organism: Homo sapiens tissue_or_cell_type: HuH-7 cells experimental_model: Cell metabolomics limitations: Pool changes alone do not quantify compartment-specific SHMT flux. exposure: Engineered ALDH1L1 expression. [sasaki-2023] One-carbon metabolizing enzyme ALDH1L1 influences mitochondrial metabolism through 5-aminoimidazole-4-carboxamide ribonucleotide accumulation and serine depletion, contributing to tumor suppression (2023). https://pubmed.ncbi.nlm.nih.gov/37596270/ DOI: 10.1038/s41598-023-38142-5
    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