Component

Human-cell mitochondrial free CoASH pool

Human-cell mitochondrial free CoASH pool

2 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 acts on it

  1. 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

  2. SLC25A42 N291D failed to restore mitochondrial CoA pools that wild-type SLC25A42 rescued.

    Human mitochondrial coenzyme A transporter SLC25A42 → 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_contrast
    {"intervention": "N291D SLC25A42 re-expression", "comparator": "Wild-type SLC25A42 re-expression in knockout cells", "endpoint": "SLC25A42 N291D failed to restore mitochondrial CoA pools that wild-type SLC25A42 rescued.", "effect_direction": "mixed", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Human K562 SLC25A42 knockout with re-expression; Fig. 6.
    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
    SLC25A42 N291D failed to restore mitochondrial CoA pools that wild-type SLC25A42 rescued.
    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-mutant-rescue; The mutant protein reached mitochondria; protein presence did not establish transport function. Mitochondrially targeted COASY also failed to restore the depleted pool.
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Acetyl-L-carnitine: detailed mechanisms of action (reviewed 6 October 2026) · lines 84–90

    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 SLC25A42 knockout with re-expression; Fig. 6. · Recorded from source · Recorded from source

    ### coa-mutant-rescue SLC25A42 N291D failed to restore mitochondrial CoA pools that wild-type SLC25A42 rescued. The mutant protein reached mitochondria; protein presence did not establish transport function. Mitochondrially targeted COASY also failed to restore the depleted pool. Model and exposure: Human K562 SLC25A42 knockout with re-expression; Fig. 6. 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.