Component

SLC25A51

Human mitochondrial NAD+ transporter.

6 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. MCART1/SLC25A51-null human cells had reduced mitochondrial NAD+/NADH, TCA-cycle flux, respiration and complex-I activity.

    SLC25A51 → Respiration supported by SLC25A51 in human cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Human cultured-cell knockout, metabolomics and isolated-mitochondrial assays.
    limitations
    Cellular transporter disruption, not proof that oral NAD crosses all membranes or treats a transporter disorder.
    nutrient_topic
    NAD+ collection; molecular form, preparation, species, exposure and manipulation remain explicit. · NAD+
    plain_language
    A functioning NAD supply outside mitochondria cannot compensate for a broken mitochondrial entry route.
    primary_references
    MCART1/SLC25A51 is required for mitochondrial NAD transport. · 2020 · https://pubmed.ncbi.nlm.nih.gov/33087354/ · DOI 10.1126/sciadv.abe5310
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    NAD+: compartmental supply, consumption and cross-nutrient mechanisms (2026-09-19) · lines 36–42

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human cultured-cell knockout, metabolomics and isolated-mitochondrial assays. · source_derived_draft · unverified_draft

    ## nad-plus-slc51-respiration A functioning NAD supply outside mitochondria cannot compensate for a broken mitochondrial entry route. MCART1/SLC25A51-null human cells had reduced mitochondrial NAD+/NADH, TCA-cycle flux, respiration and complex-I activity. Model: Human cultured-cell knockout, metabolomics and isolated-mitochondrial assays. Limitations: Cellular transporter disruption, not proof that oral NAD crosses all membranes or treats a transporter disorder. Evidence access: Primary full text MCART1/SLC25A51 is required for mitochondrial NAD transport. · 2020 · https://pubmed.ncbi.nlm.nih.gov/33087354/ · DOI 10.1126/sciadv.abe5310
    Complete structured claim and evidence

  2. Re-expression of SLC25A51 restored exogenous NAD+ uptake into mitochondria isolated from SLC25A51-deficient cells.

    SLC25A51 → Mitochondrial NAD+ uptake source_derived_draftungraded
    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": 18765, "end_char": 19491, "file_sha256": "8348dbfda6d16d576bb64301f0c75f1488e90e33c4a72213b69756bed21d047d", "text_sha256": "151d453cb71149ec656b6e82375a1e679d977643e107133d197cac4a5df0f7b9"}
    experimental_model
    HEK293T knockdown and HAP1 knockout mitochondria with genetic rescue
    exposure
    1 mM exogenous NAD+; 40-min uptake incubation
    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
    The transporter restored mitochondrial entry of intact NAD+.
    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
    Isolated mitochondria
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1029–1040

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · HEK293T knockdown and HAP1 knockout mitochondria with genetic rescue · source_derived_draft · unverified_draft

    ### b3-redox-slc25a51-import Re-expression of SLC25A51 restored exogenous NAD+ uptake into mitochondria isolated from SLC25A51-deficient cells. Condition category: machinery_impairment nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The transporter restored mitochondrial entry of intact NAD+. organism: Homo sapiens tissue_or_cell_type: Isolated mitochondria experimental_model: HEK293T knockdown and HAP1 knockout mitochondria with genetic rescue limitations: Scoped experimental observation; no dietary niacin or magnesium deficiency threshold or treatment benefit was tested. exposure: 1 mM exogenous NAD+; 40-min uptake incubation evidence_span: {"source_cache": "artifacts/niacin-redox-sources/slc25a51-2020.author.txt", "locator": "Publisher PDF, results; page/figure identified by adjacent text", "start_char": 18765, "end_char": 19491, "file_sha256": "8348dbfda6d16d576bb64301f0c75f1488e90e33c4a72213b69756bed21d047d", "text_sha256": "151d453cb71149ec656b6e82375a1e679d977643e107133d197cac4a5df0f7b9"} [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

  3. Restoration of mitochondrial NAD+ by nicotinamide riboside in the intact-cell biosensor experiment depended on SLC25A51.

    SLC25A51 → Mitochondrial NAD+ content source_derived_draftungraded
    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": 19922, "end_char": 20160, "file_sha256": "8348dbfda6d16d576bb64301f0c75f1488e90e33c4a72213b69756bed21d047d", "text_sha256": "78e9cfd3c25b8d33b54ac67bebc01314eed3925b3b6a4bdea527d48191da0977"}, {"source_cache": "artifacts/niacin-redox-sources/slc25a51-2020.author.txt", "locator": "Publisher PDF, results; page/figure identified by adjacent text", "start_char": 24477, "end_char": 24725, "file_sha256": "8348dbfda6d16d576bb64301f0c75f1488e90e33c4a72213b69756bed21d047d", "text_sha256": "7125713c87024da0a0f8c1d4442115144c9ff20543fbd39cfc4cfc46de135cad"}]
    experimental_model
    HeLa siRNA and mitochondrial NAD biosensor
    exposure
    100 μM NR for 16 h after siRNA transfection three days earlier
    limitations
    Cultured-cell precursor response; no direct clinical inference or generic claim that every NAD-raising intervention fails.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Homo sapiens
    plain_language
    Precursor provision still required functional mitochondrial import in these cells.
    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
    HeLa cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1094–1105

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · HeLa siRNA and mitochondrial NAD biosensor · source_derived_draft · unverified_draft

    ### b3-redox-slc25a51-nr-dependence Restoration of mitochondrial NAD+ by nicotinamide riboside in the intact-cell biosensor experiment depended on SLC25A51. Condition category: machinery_impairment nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Precursor provision still required functional mitochondrial import in these cells. organism: Homo sapiens tissue_or_cell_type: HeLa cells experimental_model: HeLa siRNA and mitochondrial NAD biosensor limitations: Cultured-cell precursor response; no direct clinical inference or generic claim that every NAD-raising intervention fails. exposure: 100 μM NR for 16 h after siRNA transfection three days earlier evidence_span: [{"source_cache": "artifacts/niacin-redox-sources/slc25a51-2020.author.txt", "locator": "Publisher PDF, results; page/figure identified by adjacent text", "start_char": 19922, "end_char": 20160, "file_sha256": "8348dbfda6d16d576bb64301f0c75f1488e90e33c4a72213b69756bed21d047d", "text_sha256": "78e9cfd3c25b8d33b54ac67bebc01314eed3925b3b6a4bdea527d48191da0977"}, {"source_cache": "artifacts/niacin-redox-sources/slc25a51-2020.author.txt", "locator": "Publisher PDF, results; page/figure identified by adjacent text", "start_char": 24477, "end_char": 24725, "file_sha256": "8348dbfda6d16d576bb64301f0c75f1488e90e33c4a72213b69756bed21d047d", "text_sha256": "7125713c87024da0a0f8c1d4442115144c9ff20543fbd39cfc4cfc46de135cad"}] [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

Where it participates (unsigned role)

  1. SLC25A51 loss reduced mitochondrial NAD+ availability in the tested human cell models.

    SLC25A51 depletion or knockout → Mitochondrial NAD+ content source_derived_draftungraded
    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 evidence

  2. Unlike NAD+, exogenous nicotinamide or NMN did not replenish matrix NAD+ in the isolated-mitochondrial assay.

    Nicotinamide → Mitochondrial NAD+ content source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/niacin-redox-sources/slc25a51-2020.author.txt", "locator": "Publisher PDF, results; page/figure identified by adjacent text", "start_char": 18765, "end_char": 19225, "file_sha256": "8348dbfda6d16d576bb64301f0c75f1488e90e33c4a72213b69756bed21d047d", "text_sha256": "121f48fd5cc272acc24a9ca1610c801423a98e3e44f7851e649c8454750e7fb0"}
    experimental_model
    Isolated mitochondria substrate comparison
    exposure
    Exogenous NAD+, nicotinamide or NMN
    limitations
    Does not imply oral NAM/NMN cannot contribute to mitochondrial NAD after extramitochondrial metabolism; this is an isolated-organelle test.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Homo sapiens
    plain_language
    These precursors were not interchangeable with intact NAD in this uptake experiment.
    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
    Isolated human-cell mitochondria

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1068–1079

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

    ### b3-redox-slc25a51-nam-nmn-null Unlike NAD+, exogenous nicotinamide or NMN did not replenish matrix NAD+ in the isolated-mitochondrial assay. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: These precursors were not interchangeable with intact NAD in this uptake experiment. organism: Homo sapiens tissue_or_cell_type: Isolated human-cell mitochondria experimental_model: Isolated mitochondria substrate comparison limitations: Does not imply oral NAM/NMN cannot contribute to mitochondrial NAD after extramitochondrial metabolism; this is an isolated-organelle test. exposure: Exogenous NAD+, nicotinamide or NMN evidence_span: {"source_cache": "artifacts/niacin-redox-sources/slc25a51-2020.author.txt", "locator": "Publisher PDF, results; page/figure identified by adjacent text", "start_char": 18765, "end_char": 19225, "file_sha256": "8348dbfda6d16d576bb64301f0c75f1488e90e33c4a72213b69756bed21d047d", "text_sha256": "121f48fd5cc272acc24a9ca1610c801423a98e3e44f7851e649c8454750e7fb0"} [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

  3. Excess NMN or nicotinamide did not compete with NAD+ uptake in the isolated-mitochondrial competition assay.

    NMN → Mitochondrial NAD+ uptake source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/niacin-redox-sources/slc25a51-2020.author.txt", "locator": "Publisher PDF, results; page/figure identified by adjacent text", "start_char": 19115, "end_char": 19225, "file_sha256": "8348dbfda6d16d576bb64301f0c75f1488e90e33c4a72213b69756bed21d047d", "text_sha256": "71f08e5c405c67340bfbe5e1d027cebc9c0f37a2e64bdbd4205020f1ee23e005"}
    experimental_model
    Competition assay with isolated human-cell mitochondria
    exposure
    Excess precursor alongside NAD+
    limitations
    Assay-specific negative competition; no assertion that every derivative is excluded from all transporters.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Homo sapiens
    plain_language
    The two precursors did not block the measured NAD import route.
    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
    Mitochondria

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1081–1092

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Competition assay with isolated human-cell mitochondria · source_derived_draft · unverified_draft

    ### b3-redox-slc25a51-precursor-competition-null Excess NMN or nicotinamide did not compete with NAD+ uptake in the isolated-mitochondrial competition assay. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The two precursors did not block the measured NAD import route. organism: Homo sapiens tissue_or_cell_type: Mitochondria experimental_model: Competition assay with isolated human-cell mitochondria limitations: Assay-specific negative competition; no assertion that every derivative is excluded from all transporters. exposure: Excess precursor alongside NAD+ evidence_span: {"source_cache": "artifacts/niacin-redox-sources/slc25a51-2020.author.txt", "locator": "Publisher PDF, results; page/figure identified by adjacent text", "start_char": 19115, "end_char": 19225, "file_sha256": "8348dbfda6d16d576bb64301f0c75f1488e90e33c4a72213b69756bed21d047d", "text_sha256": "71f08e5c405c67340bfbe5e1d027cebc9c0f37a2e64bdbd4205020f1ee23e005"} [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

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.

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