Component

SLC25A48-deficient human cells in the 2024 transport studies

SLC25A48-deficient human cells in the 2024 transport studies. 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.

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. SLC25A48 loss impaired choline-derived betaine production in human-cell mitochondrial metabolism experiments.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/choline-research/39111307.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0a9377732782bdaa55105cae0a0446afcfb1225e686d2b047a7fdf1ef67535f", "start_char": 0, "end_char": 1201, "text_sha256": "c0a9377732782bdaa55105cae0a0446afcfb1225e686d2b047a7fdf1ef67535f"}
    experimental_model
    Slc25a48 knockout, rescue, mitochondrial assays and isotope tracing
    exposure
    Germline mouse knockout; human-cell SLC25A48 loss; labeled choline
    limitations
    Transport, energy and one-carbon outcomes are model-specific; normal intake cannot be assumed to correct a carrier defect.
    nutrient_topic
    Choline research collection; topical membership is not evidence of a direct dietary effect. · Choline
    organism
    Human HEK293T cells
    plain_language
    A transport defect can restrict methyl-donor production upstream of betaine.
    primary_references
    [choline-p39111307] SLC25A48 controls mitochondrial choline import and metabolism. (2024). https://pubmed.ncbi.nlm.nih.gov/39111307/ DOI: 10.1016/j.cmet.2024.07.010
    tissue_or_cell_type
    Brown adipose tissue and human HEK293T cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Choline: metabolism, signaling and nutrient connections (2026-09-17) · lines 490–501

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Slc25a48 knockout, rescue, mitochondrial assays and isotope tracing · source_derived_draft · unverified_draft

    ### choline-slc25a48-betaine SLC25A48 loss impaired choline-derived betaine production in human-cell mitochondrial metabolism experiments. Condition category: machinery_impairment nutrient_topic: Choline research collection; topical membership is not evidence of a direct dietary effect. plain_language: A transport defect can restrict methyl-donor production upstream of betaine. organism: Human HEK293T cells tissue_or_cell_type: Brown adipose tissue and human HEK293T cells experimental_model: Slc25a48 knockout, rescue, mitochondrial assays and isotope tracing limitations: Transport, energy and one-carbon outcomes are model-specific; normal intake cannot be assumed to correct a carrier defect. exposure: Germline mouse knockout; human-cell SLC25A48 loss; labeled choline evidence_span: {"source_cache": "artifacts/choline-research/39111307.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0a9377732782bdaa55105cae0a0446afcfb1225e686d2b047a7fdf1ef67535f", "start_char": 0, "end_char": 1201, "text_sha256": "c0a9377732782bdaa55105cae0a0446afcfb1225e686d2b047a7fdf1ef67535f"} [choline-p39111307] SLC25A48 controls mitochondrial choline import and metabolism. (2024). https://pubmed.ncbi.nlm.nih.gov/39111307/ DOI: 10.1016/j.cmet.2024.07.010
    Complete structured claim and evidence
  2. SLC25A48 loss reduced the contribution of labeled choline to purine nucleotides in HEK293T cells.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/choline-research/39111307.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0a9377732782bdaa55105cae0a0446afcfb1225e686d2b047a7fdf1ef67535f", "start_char": 0, "end_char": 1201, "text_sha256": "c0a9377732782bdaa55105cae0a0446afcfb1225e686d2b047a7fdf1ef67535f"}
    experimental_model
    Slc25a48 knockout, rescue, mitochondrial assays and isotope tracing
    exposure
    1 mM 13C2-choline for 24 hours in the study methods
    limitations
    Tracer contribution is not a claim that choline directly becomes a whole nucleotide or that dietary choline controls every purine pathway.
    nutrient_topic
    Choline research collection; topical membership is not evidence of a direct dietary effect. · Choline
    organism
    Human HEK293T cells
    plain_language
    Choline-derived metabolism reached nucleotide production in the tracer experiment.
    primary_references
    [choline-p39111307] SLC25A48 controls mitochondrial choline import and metabolism. (2024). https://pubmed.ncbi.nlm.nih.gov/39111307/ DOI: 10.1016/j.cmet.2024.07.010
    tissue_or_cell_type
    Brown adipose tissue and human HEK293T cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Choline: metabolism, signaling and nutrient connections (2026-09-17) · lines 503–514

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Slc25a48 knockout, rescue, mitochondrial assays and isotope tracing · source_derived_draft · unverified_draft

    ### choline-slc25a48-purines SLC25A48 loss reduced the contribution of labeled choline to purine nucleotides in HEK293T cells. Condition category: machinery_impairment nutrient_topic: Choline research collection; topical membership is not evidence of a direct dietary effect. plain_language: Choline-derived metabolism reached nucleotide production in the tracer experiment. organism: Human HEK293T cells tissue_or_cell_type: Brown adipose tissue and human HEK293T cells experimental_model: Slc25a48 knockout, rescue, mitochondrial assays and isotope tracing limitations: Tracer contribution is not a claim that choline directly becomes a whole nucleotide or that dietary choline controls every purine pathway. exposure: 1 mM 13C2-choline for 24 hours in the study methods evidence_span: {"source_cache": "artifacts/choline-research/39111307.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0a9377732782bdaa55105cae0a0446afcfb1225e686d2b047a7fdf1ef67535f", "start_char": 0, "end_char": 1201, "text_sha256": "c0a9377732782bdaa55105cae0a0446afcfb1225e686d2b047a7fdf1ef67535f"} [choline-p39111307] SLC25A48 controls mitochondrial choline import and metabolism. (2024). https://pubmed.ncbi.nlm.nih.gov/39111307/ DOI: 10.1016/j.cmet.2024.07.010
    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