Component
SLC25A51 depletion or knockout
Experimental human SLC25A51 loss by RNA interference or CRISPR knockout; exact method retained per 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
SLC25A51 loss reduced mitochondrial NAD+ availability in the tested human cell models.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/niacin-redox-sources/slc25a51-2020.author.txt", "locator": "Publisher PDF, results; page/figure identified by adjacent text", "start_char": 6119, "end_char": 6538, "file_sha256": "8348dbfda6d16d576bb64301f0c75f1488e90e33c4a72213b69756bed21d047d", "text_sha256": "024f4688a65e3279f2865ef892f19ed4d5357469c71a5e2e6fb27fe1a2dd4043"}
- experimental_model
- Multiple shRNA/siRNA perturbations; mitochondrial assays and biosensors
- exposure
- SLC25A51 RNA interference
- limitations
- Scoped experimental observation; no dietary niacin or magnesium deficiency threshold or treatment benefit was tested.
- nutrient_topic
- Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
- organism
- Homo sapiens
- plain_language
- Cells can lose mitochondrial NAD even when the total-cell pool is maintained.
- primary_references
- [slc25a51-2020] SLC25A51 is a mammalian mitochondrial NAD+ transporter. (2020). https://pubmed.ncbi.nlm.nih.gov/32906142/ DOI: 10.1038/s41586-020-2741-7
- tissue_or_cell_type
- Human cultured cells
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1042–1053
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Multiple shRNA/siRNA perturbations; mitochondrial assays and biosensors · source_derived_draft · unverified_draft
### b3-redox-slc25a51-mito-pool SLC25A51 loss reduced mitochondrial NAD+ availability in the tested human cell models. Condition category: machinery_impairment nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Cells can lose mitochondrial NAD even when the total-cell pool is maintained. organism: Homo sapiens tissue_or_cell_type: Human cultured cells experimental_model: Multiple shRNA/siRNA perturbations; mitochondrial assays and biosensors limitations: Scoped experimental observation; no dietary niacin or magnesium deficiency threshold or treatment benefit was tested. exposure: SLC25A51 RNA interference evidence_span: {"source_cache": "artifacts/niacin-redox-sources/slc25a51-2020.author.txt", "locator": "Publisher PDF, results; page/figure identified by adjacent text", "start_char": 6119, "end_char": 6538, "file_sha256": "8348dbfda6d16d576bb64301f0c75f1488e90e33c4a72213b69756bed21d047d", "text_sha256": "024f4688a65e3279f2865ef892f19ed4d5357469c71a5e2e6fb27fe1a2dd4043"} [slc25a51-2020] SLC25A51 is a mammalian mitochondrial NAD+ transporter. (2020). https://pubmed.ncbi.nlm.nih.gov/32906142/ DOI: 10.1038/s41586-020-2741-7
Complete structured claim and evidenceSLC25A51 loss did not reduce whole-cell NAD+ content in the comparisons that showed mitochondrial depletion.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/niacin-redox-sources/slc25a51-2020.author.txt", "locator": "Publisher PDF, results; page/figure identified by adjacent text", "start_char": 6119, "end_char": 6538, "file_sha256": "8348dbfda6d16d576bb64301f0c75f1488e90e33c4a72213b69756bed21d047d", "text_sha256": "024f4688a65e3279f2865ef892f19ed4d5357469c71a5e2e6fb27fe1a2dd4043"}
- experimental_model
- RNA interference and whole-cell NAD measurements
- exposure
- SLC25A51 depletion
- limitations
- Scoped null result; total NAD is not a universal proxy for mitochondrial NAD availability.
- nutrient_topic
- Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
- organism
- Homo sapiens
- plain_language
- A total-cell measurement did not reveal the compartment-specific deficit.
- primary_references
- [slc25a51-2020] SLC25A51 is a mammalian mitochondrial NAD+ transporter. (2020). https://pubmed.ncbi.nlm.nih.gov/32906142/ DOI: 10.1038/s41586-020-2741-7
- tissue_or_cell_type
- Human cell lines
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1055–1066
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · RNA interference and whole-cell NAD measurements · source_derived_draft · unverified_draft
### b3-redox-slc25a51-whole-cell-null SLC25A51 loss did not reduce whole-cell NAD+ content in the comparisons that showed mitochondrial depletion. Condition category: machinery_impairment nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A total-cell measurement did not reveal the compartment-specific deficit. organism: Homo sapiens tissue_or_cell_type: Human cell lines experimental_model: RNA interference and whole-cell NAD measurements limitations: Scoped null result; total NAD is not a universal proxy for mitochondrial NAD availability. exposure: SLC25A51 depletion evidence_span: {"source_cache": "artifacts/niacin-redox-sources/slc25a51-2020.author.txt", "locator": "Publisher PDF, results; page/figure identified by adjacent text", "start_char": 6119, "end_char": 6538, "file_sha256": "8348dbfda6d16d576bb64301f0c75f1488e90e33c4a72213b69756bed21d047d", "text_sha256": "024f4688a65e3279f2865ef892f19ed4d5357469c71a5e2e6fb27fe1a2dd4043"} [slc25a51-2020] SLC25A51 is a mammalian mitochondrial NAD+ transporter. (2020). https://pubmed.ncbi.nlm.nih.gov/32906142/ DOI: 10.1038/s41586-020-2741-7
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.