Component
Human mitochondrial choline carrier SLC25A48
Human mitochondrial choline carrier SLC25A48. 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.
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 it acts on
Human-cell experiments identified SLC25A48 as necessary for efficient mitochondrial choline import.
Experimental context and source evidence
- 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
- Choline must cross another membrane to reach its mitochondrial metabolic route.
- 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
Choline: metabolism, signaling and nutrient connections (2026-09-17) · lines 477–488
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-import Human-cell experiments identified SLC25A48 as necessary for efficient mitochondrial choline import. Condition category: normal nutrient_topic: Choline research collection; topical membership is not evidence of a direct dietary effect. plain_language: Choline must cross another membrane to reach its mitochondrial metabolic route. 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 evidenceAn independent GeneMAP study found that SLC25A48 loss strongly impaired mitochondrial choline import.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/choline-research/38977856.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "80a5e7038c33442cc887901558cb662b39fe4c54e3821f860c12a388c8a44c92", "start_char": 0, "end_char": 1169, "text_sha256": "80a5e7038c33442cc887901558cb662b39fe4c54e3821f860c12a388c8a44c92"}
- experimental_model
- Independent gene–metabolite mapping and mitochondrial experiments
- exposure
- SLC25A48 genetic association and loss-of-function experiments
- limitations
- Indexed abstract leaves individual construct details unresolved; no tissue-specific quantitative claim is made here.
- nutrient_topic
- Choline research collection; topical membership is not evidence of a direct dietary effect. · Choline
- organism
- Human genetic data and experimental cells
- plain_language
- A second research group supported the same transport step.
- primary_references
- [choline-p38977856] Metabolic gene function discovery platform GeneMAP identifies SLC25A48 as necessary for mitochondrial choline import. (2024). https://pubmed.ncbi.nlm.nih.gov/38977856/ DOI: 10.1038/s41588-024-01827-2
- tissue_or_cell_type
- Plasma choline and mitochondrial import
Choline: metabolism, signaling and nutrient connections (2026-09-17) · lines 555–566
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Independent gene–metabolite mapping and mitochondrial experiments · source_derived_draft · unverified_draft
### choline-slc25a48-independent An independent GeneMAP study found that SLC25A48 loss strongly impaired mitochondrial choline import. Condition category: normal nutrient_topic: Choline research collection; topical membership is not evidence of a direct dietary effect. plain_language: A second research group supported the same transport step. organism: Human genetic data and experimental cells tissue_or_cell_type: Plasma choline and mitochondrial import experimental_model: Independent gene–metabolite mapping and mitochondrial experiments limitations: Indexed abstract leaves individual construct details unresolved; no tissue-specific quantitative claim is made here. exposure: SLC25A48 genetic association and loss-of-function experiments evidence_span: {"source_cache": "artifacts/choline-research/38977856.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "80a5e7038c33442cc887901558cb662b39fe4c54e3821f860c12a388c8a44c92", "start_char": 0, "end_char": 1169, "text_sha256": "80a5e7038c33442cc887901558cb662b39fe4c54e3821f860c12a388c8a44c92"} [choline-p38977856] Metabolic gene function discovery platform GeneMAP identifies SLC25A48 as necessary for mitochondrial choline import. (2024). https://pubmed.ncbi.nlm.nih.gov/38977856/ DOI: 10.1038/s41588-024-01827-2
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.