Component

Human mitochondrial CoA transporter SLC25A16

Human mitochondrial CoA transporter SLC25A16

3 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. Combined SLC25A16/SLC25A42 deletion impaired fatty-acid oxidation and shifted TCA labeling toward reductive routes.

    Human mitochondrial CoA transporter SLC25A16 → Human-cell fatty-acid oxidation during impaired CoA import Recorded from sourceungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    experimental_condition
    Control cells deleted · Human mitochondrial CoA transporter SLC25A16 Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_condition
    Control cells deleted · Human mitochondrial coenzyme A transporter SLC25A42 Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "SLC25A16 and SLC25A42 double knockout", "comparator": "Control cells", "endpoint": "Combined SLC25A16/SLC25A42 deletion impaired fatty-acid oxidation and shifted TCA labeling toward reductive routes.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "human-slc25a16", "state": "deleted"}, {"entity_slug": "slc25a42", "state": "deleted"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    K562 and HeLa cells; mitochondrial metabolomics, respiration and 13C5-glutamine tracing.
    interpretation_status
    Source-derived curation with stated access limits; ungraded, not independent replication.
    limitations
    Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
    nutrient_topic
    Acetyl-L-carnitine collection; exact intervention and molecular form govern interpretation. · Acetyl-L-carnitine
    plain_language
    Combined SLC25A16/SLC25A42 deletion impaired fatty-acid oxidation and shifted TCA labeling toward reductive routes.
    primary_references
    Cellular pan-chain acyl-CoA profiling reveals SLC25A42/SLC25A16 in mitochondrial CoA import and metabolism. | https://pubmed.ncbi.nlm.nih.gov/40925986/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC12460162/ | https://doi.org/10.1038/s42255-025-01358-y
    source_locator
    Reviewed reference coa-import-fao; Long-chain acylcarnitines accumulated while free CoA fell. More acyl carrier is not equivalent to restored matrix CoA. ALCAR supplementation was not tested as rescue in this comparison.
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Acetyl-L-carnitine: detailed mechanisms of action (reviewed 6 October 2026) · lines 68–74

    AI-assisted original review of primary studies and clearly identified official records. Exact primary access is stated; no independent replication is claimed. · supports · K562 and HeLa cells; mitochondrial metabolomics, respiration and 13C5-glutamine tracing. · Recorded from source · Recorded from source

    ### coa-import-fao Combined SLC25A16/SLC25A42 deletion impaired fatty-acid oxidation and shifted TCA labeling toward reductive routes. Long-chain acylcarnitines accumulated while free CoA fell. More acyl carrier is not equivalent to restored matrix CoA. ALCAR supplementation was not tested as rescue in this comparison. Model and exposure: K562 and HeLa cells; mitochondrial metabolomics, respiration and 13C5-glutamine tracing. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Cellular pan-chain acyl-CoA profiling reveals SLC25A42/SLC25A16 in mitochondrial CoA import and metabolism. | 2025 | https://pubmed.ncbi.nlm.nih.gov/40925986/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC12460162/ | https://doi.org/10.1038/s42255-025-01358-y | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    Complete structured claim and evidence

  2. Combined SLC25A16/SLC25A42 deletion depleted mitochondrial free CoASH in human K562 and HeLa cells.

    Human mitochondrial CoA transporter SLC25A16 → Human-cell mitochondrial free CoASH pool Recorded from sourceungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    experimental_condition
    Matched control cells deleted · Human mitochondrial CoA transporter SLC25A16 Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_condition
    Matched control cells deleted · Human mitochondrial coenzyme A transporter SLC25A42 Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "SLC25A16 and SLC25A42 double knockout", "comparator": "Matched control cells", "endpoint": "Combined SLC25A16/SLC25A42 deletion depleted mitochondrial free CoASH in human K562 and HeLa cells.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "human-slc25a16", "state": "deleted"}, {"entity_slug": "slc25a42", "state": "deleted"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Human K562/HeLa double-knockout cells; mitochondrial isolation and LC-MS; Figs 4–7.
    interpretation_status
    Source-derived curation with stated access limits; ungraded, not independent replication.
    limitations
    Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
    nutrient_topic
    Acetyl-L-carnitine collection; exact intervention and molecular form govern interpretation. · Acetyl-L-carnitine
    plain_language
    Combined SLC25A16/SLC25A42 deletion depleted mitochondrial free CoASH in human K562 and HeLa cells.
    primary_references
    Cellular pan-chain acyl-CoA profiling reveals SLC25A42/SLC25A16 in mitochondrial CoA import and metabolism. | https://pubmed.ncbi.nlm.nih.gov/40925986/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC12460162/ | https://doi.org/10.1038/s42255-025-01358-y
    source_locator
    Reviewed reference coa-import-joint; Loss of both transporters also depleted several matrix-enriched short-chain acyl-CoAs. Stable-isotope CoASH uptake was reduced. Do not split this double-knockout result into two independent single-gene effects.
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Acetyl-L-carnitine: detailed mechanisms of action (reviewed 6 October 2026) · lines 60–66

    AI-assisted original review of primary studies and clearly identified official records. Exact primary access is stated; no independent replication is claimed. · supports · Human K562/HeLa double-knockout cells; mitochondrial isolation and LC-MS; Figs 4–7. · Recorded from source · Recorded from source

    ### coa-import-joint Combined SLC25A16/SLC25A42 deletion depleted mitochondrial free CoASH in human K562 and HeLa cells. Loss of both transporters also depleted several matrix-enriched short-chain acyl-CoAs. Stable-isotope CoASH uptake was reduced. Do not split this double-knockout result into two independent single-gene effects. Model and exposure: Human K562/HeLa double-knockout cells; mitochondrial isolation and LC-MS; Figs 4–7. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Cellular pan-chain acyl-CoA profiling reveals SLC25A42/SLC25A16 in mitochondrial CoA import and metabolism. | 2025 | https://pubmed.ncbi.nlm.nih.gov/40925986/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC12460162/ | https://doi.org/10.1038/s42255-025-01358-y | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Labeled pantothenate supplied the CoA backbone used to trace mitochondrial CoASH import in human cells.

    Pantothenate (vitamin B5) → Coenzyme A Recorded from sourceungraded
    Experimental context and source evidence
    evidence_access
    Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    experimental_model
    Human K562 cells; 13C3-15N-pantothenate labeling for three days followed by acyl-CoA extraction and mitochondrial uptake assay; Fig. 7a.
    interpretation_status
    Source-derived curation with stated access limits; ungraded, not independent replication.
    limitations
    Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
    nutrient_topic
    Acetyl-L-carnitine collection; exact intervention and molecular form govern interpretation. · Acetyl-L-carnitine
    plain_language
    Labeled pantothenate supplied the CoA backbone used to trace mitochondrial CoASH import in human cells.
    primary_references
    Cellular pan-chain acyl-CoA profiling reveals SLC25A42/SLC25A16 in mitochondrial CoA import and metabolism. | https://pubmed.ncbi.nlm.nih.gov/40925986/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC12460162/ | https://doi.org/10.1038/s42255-025-01358-y
    source_locator
    Reviewed reference b5-coa-backbone; The isotope labels were on the CoA moiety, not its attached acetyl group. This connects vitamin B5 supply to the cofactor required for ALCAR use without asserting a benefit from excess B5.

    Acetyl-L-carnitine: detailed mechanisms of action (reviewed 6 October 2026) · lines 52–58

    AI-assisted original review of primary studies and clearly identified official records. Exact primary access is stated; no independent replication is claimed. · supports · Human K562 cells; 13C3-15N-pantothenate labeling for three days followed by acyl-CoA extraction and mitochondrial uptake assay; Fig. 7a. · Recorded from source · Recorded from source

    ### b5-coa-backbone Labeled pantothenate supplied the CoA backbone used to trace mitochondrial CoASH import in human cells. The isotope labels were on the CoA moiety, not its attached acetyl group. This connects vitamin B5 supply to the cofactor required for ALCAR use without asserting a benefit from excess B5. Model and exposure: Human K562 cells; 13C3-15N-pantothenate labeling for three days followed by acyl-CoA extraction and mitochondrial uptake assay; Fig. 7a. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Cellular pan-chain acyl-CoA profiling reveals SLC25A42/SLC25A16 in mitochondrial CoA import and metabolism. | 2025 | https://pubmed.ncbi.nlm.nih.gov/40925986/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC12460162/ | https://doi.org/10.1038/s42255-025-01358-y | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    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.