Component

Acetyl-lysine signal on experimental HADHA constructs

Study-specific entity. Experimental conditions and evidence limits remain on each linked claim.

4 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

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How nutrients influence it

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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.

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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. Omitting acetyl-CoA prevented the Dlat-associated HADHA acetylation signal in the purified-protein assay.

    Acetyl-CoA → Acetyl-lysine signal on experimental HADHA constructs source_derived_draftungraded
    Experimental context and source evidence
    access_level
    full_text_and_supplement_review
    compartment
    In vitro reaction, not an intact-cell compartment
    dose
    Acetyl-CoA present/absent controls; concentrations and incubation details incompletely specified
    duration
    Not specified in the reviewed methods
    endpoint
    hadha-construct-lysine-acetylation
    evidence_location
    Acetyl-CoA omission control; Figure 6J
    experimental_model
    Recombinant-protein acetylation assay
    exposure
    acetyl-coa
    limitations
    Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. This is an omission-control observation, not a dietary or intracellular acetyl-CoA threshold.
    organism
    Recombinant mouse Dlat; HADHA construct sequence species unresolved in reviewed methods
    plain_language
    Omitting acetyl-CoA prevented the Dlat-associated HADHA acetylation signal in the purified-protein assay.
    primary_locator
    [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 44, "text_sha256": "e0a92f47bc76c894816706ffb5158242c968928ac61e4561262c370035eda621", "xml_element_id": "Par19"}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 46, "text_sha256": "d56a90702bdf004de1efc2e43103b1b771e15b38288dc01f3741676782b1f5ff", "xml_element_id": null}]
    primary_references
    https://doi.org/10.1038/s41467-026-70703-w
    sample_size
    4 biological replicates
    tissue_or_cell_type
    Purified-protein reaction

    DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 70–85

    AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Recombinant-protein acetylation assay · source_derived_draft · unverified_draft

    Omitting acetyl-CoA prevented the Dlat-associated HADHA acetylation signal in the purified-protein assay. organism: Recombinant mouse Dlat; HADHA construct sequence species unresolved in reviewed methods tissue_or_cell_type: Purified-protein reaction experimental_model: Recombinant-protein acetylation assay compartment: In vitro reaction, not an intact-cell compartment dose: Acetyl-CoA present/absent controls; concentrations and incubation details incompletely specified duration: Not specified in the reviewed methods primary_references: https://doi.org/10.1038/s41467-026-70703-w access_level: full_text_and_supplement_review evidence_location: Acetyl-CoA omission control; Figure 6J endpoint: hadha-construct-lysine-acetylation exposure: acetyl-coa limitations: Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. This is an omission-control observation, not a dietary or intracellular acetyl-CoA threshold. primary_locator: [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 44, "text_sha256": "e0a92f47bc76c894816706ffb5158242c968928ac61e4561262c370035eda621", "xml_element_id": "Par19"}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 46, "text_sha256": "d56a90702bdf004de1efc2e43103b1b771e15b38288dc01f3741676782b1f5ff", "xml_element_id": null}] plain_language: Omitting acetyl-CoA prevented the Dlat-associated HADHA acetylation signal in the purified-protein assay. sample_size: 4 biological replicates
    Complete structured claim and evidence

  2. The K728R HADHA construct resisted the Dlat-induced increase in acetyl-lysine signal in HEK293 experiments.

    HADHA K728R experimental construct → Acetyl-lysine signal on experimental HADHA constructs source_derived_draftungraded
    Experimental context and source evidence
    access_level
    full_text_and_supplement_review
    compartment
    Immunoprecipitated tagged protein
    dose
    Construct amounts not specified in reviewed text
    duration
    Not specified in reviewed text
    endpoint
    hadha-construct-lysine-acetylation
    evidence_location
    Flag immunoprecipitation/acetyl-lysine blot; Figure 7D/F
    experimental_model
    Flag-HADHA point-mutant/combined-mutant transfection
    exposure
    hadha-k728r-construct
    limitations
    Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. K728R removes the lysine: this blot does not measure acetylation at residue 728. Other-site and structural effects remain possible; peer-review response pp.9–10.
    organism
    Homo sapiens HEK293 host; construct sequence species not assumed from host
    plain_language
    The K728R HADHA construct resisted the Dlat-induced increase in acetyl-lysine signal in HEK293 experiments.
    primary_locator
    [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 48, "text_sha256": "134dcda50e7eafd608062a092c3cab71e5febe5935586f7d7d478988d6a3ea8e", "xml_element_id": "Par20"}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 50, "text_sha256": "ef3c37a398cc33c2cac08d4fc06ef96648c5fcda5ce3de26387b1afb609af2bf", "xml_element_id": null}, {"cache": "artifacts/dlat-curation/41467_2026_70703_MOESM3_ESM.pdf", "location": "PDF pages 9-10 and 16-17; concern and subsequent additional controls", "sha256": "79ca0576c4b70ef33a468724c6ec9f2ed75041428536ec0e2444561ee575b865"}]
    primary_references
    https://doi.org/10.1038/s41467-026-70703-w
    sample_size
    4 per group
    tissue_or_cell_type
    HEK293 cells

    DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 106–121

    AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Flag-HADHA point-mutant/combined-mutant transfection · source_derived_draft · unverified_draft

    The K728R HADHA construct resisted the Dlat-induced increase in acetyl-lysine signal in HEK293 experiments. organism: Homo sapiens HEK293 host; construct sequence species not assumed from host tissue_or_cell_type: HEK293 cells experimental_model: Flag-HADHA point-mutant/combined-mutant transfection compartment: Immunoprecipitated tagged protein dose: Construct amounts not specified in reviewed text duration: Not specified in reviewed text primary_references: https://doi.org/10.1038/s41467-026-70703-w access_level: full_text_and_supplement_review evidence_location: Flag immunoprecipitation/acetyl-lysine blot; Figure 7D/F endpoint: hadha-construct-lysine-acetylation exposure: hadha-k728r-construct limitations: Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. K728R removes the lysine: this blot does not measure acetylation at residue 728. Other-site and structural effects remain possible; peer-review response pp.9–10. primary_locator: [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 48, "text_sha256": "134dcda50e7eafd608062a092c3cab71e5febe5935586f7d7d478988d6a3ea8e", "xml_element_id": "Par20"}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 50, "text_sha256": "ef3c37a398cc33c2cac08d4fc06ef96648c5fcda5ce3de26387b1afb609af2bf", "xml_element_id": null}, {"cache": "artifacts/dlat-curation/41467_2026_70703_MOESM3_ESM.pdf", "location": "PDF pages 9-10 and 16-17; concern and subsequent additional controls", "sha256": "79ca0576c4b70ef33a468724c6ec9f2ed75041428536ec0e2444561ee575b865"}] plain_language: The K728R HADHA construct resisted the Dlat-induced increase in acetyl-lysine signal in HEK293 experiments. sample_size: 4 per group
    Complete structured claim and evidence

  3. Dlat produced no detectable acetyl-lysine signal on the tested recombinant K728R HADHA construct.

    HADHA K728R experimental construct → Acetyl-lysine signal on experimental HADHA constructs source_derived_draftungraded
    Experimental context and source evidence
    access_level
    full_text_and_supplement_review
    compartment
    In vitro reaction, not an intact-cell compartment
    dose
    Acetyl-CoA present/absent controls; concentrations and incubation details incompletely specified
    duration
    Not specified in the reviewed methods
    endpoint
    hadha-construct-lysine-acetylation
    evidence_location
    Figure 7E
    experimental_model
    Recombinant-protein acetylation assay
    exposure
    hadha-k728r-construct
    limitations
    Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. A construct-dependent result, not direct residue-specific occupancy quantification or a mouse-heart mutant experiment.
    organism
    Recombinant mouse Dlat; HADHA construct sequence species unresolved in reviewed methods
    plain_language
    Dlat produced no detectable acetyl-lysine signal on the tested recombinant K728R HADHA construct.
    primary_locator
    [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 48, "text_sha256": "134dcda50e7eafd608062a092c3cab71e5febe5935586f7d7d478988d6a3ea8e", "xml_element_id": "Par20"}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 50, "text_sha256": "ef3c37a398cc33c2cac08d4fc06ef96648c5fcda5ce3de26387b1afb609af2bf", "xml_element_id": null}]
    primary_references
    https://doi.org/10.1038/s41467-026-70703-w
    sample_size
    4 biological replicates
    tissue_or_cell_type
    Purified-protein reaction

    DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 142–157

    AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Recombinant-protein acetylation assay · source_derived_draft · unverified_draft

    Dlat produced no detectable acetyl-lysine signal on the tested recombinant K728R HADHA construct. organism: Recombinant mouse Dlat; HADHA construct sequence species unresolved in reviewed methods tissue_or_cell_type: Purified-protein reaction experimental_model: Recombinant-protein acetylation assay compartment: In vitro reaction, not an intact-cell compartment dose: Acetyl-CoA present/absent controls; concentrations and incubation details incompletely specified duration: Not specified in the reviewed methods primary_references: https://doi.org/10.1038/s41467-026-70703-w access_level: full_text_and_supplement_review evidence_location: Figure 7E endpoint: hadha-construct-lysine-acetylation exposure: hadha-k728r-construct limitations: Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. A construct-dependent result, not direct residue-specific occupancy quantification or a mouse-heart mutant experiment. primary_locator: [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 48, "text_sha256": "134dcda50e7eafd608062a092c3cab71e5febe5935586f7d7d478988d6a3ea8e", "xml_element_id": "Par20"}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 50, "text_sha256": "ef3c37a398cc33c2cac08d4fc06ef96648c5fcda5ce3de26387b1afb609af2bf", "xml_element_id": null}] plain_language: Dlat produced no detectable acetyl-lysine signal on the tested recombinant K728R HADHA construct. sample_size: 4 biological replicates
    Complete structured claim and evidence

  4. The HADHA 350/383/406 triple mutant remained susceptible to Dlat-induced acetylation in HEK293 cells.

    HADHA TRIPLE-350-383-406 experimental construct → Acetyl-lysine signal on experimental HADHA constructs source_derived_draftungraded
    Experimental context and source evidence
    access_level
    full_text_and_supplement_review
    compartment
    Immunoprecipitated tagged protein
    dose
    Construct amounts not specified in reviewed text
    duration
    Not specified in reviewed text
    endpoint
    hadha-construct-lysine-acetylation
    evidence_location
    Figure 7F
    experimental_model
    Flag-HADHA point-mutant/combined-mutant transfection
    exposure
    hadha-triple-350-383-406-construct
    limitations
    Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. The negative control is limited to the tested substitutions; it does not exclude all other cooperating residues.
    organism
    Homo sapiens HEK293 host; construct sequence species not assumed from host
    plain_language
    The HADHA 350/383/406 triple mutant remained susceptible to Dlat-induced acetylation in HEK293 cells.
    primary_locator
    [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 48, "text_sha256": "134dcda50e7eafd608062a092c3cab71e5febe5935586f7d7d478988d6a3ea8e", "xml_element_id": "Par20"}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 50, "text_sha256": "ef3c37a398cc33c2cac08d4fc06ef96648c5fcda5ce3de26387b1afb609af2bf", "xml_element_id": null}]
    primary_references
    https://doi.org/10.1038/s41467-026-70703-w
    sample_size
    4 per group
    tissue_or_cell_type
    HEK293 cells

    DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 124–139

    AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Flag-HADHA point-mutant/combined-mutant transfection · source_derived_draft · unverified_draft

    The HADHA 350/383/406 triple mutant remained susceptible to Dlat-induced acetylation in HEK293 cells. organism: Homo sapiens HEK293 host; construct sequence species not assumed from host tissue_or_cell_type: HEK293 cells experimental_model: Flag-HADHA point-mutant/combined-mutant transfection compartment: Immunoprecipitated tagged protein dose: Construct amounts not specified in reviewed text duration: Not specified in reviewed text primary_references: https://doi.org/10.1038/s41467-026-70703-w access_level: full_text_and_supplement_review evidence_location: Figure 7F endpoint: hadha-construct-lysine-acetylation exposure: hadha-triple-350-383-406-construct limitations: Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. The negative control is limited to the tested substitutions; it does not exclude all other cooperating residues. primary_locator: [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 48, "text_sha256": "134dcda50e7eafd608062a092c3cab71e5febe5935586f7d7d478988d6a3ea8e", "xml_element_id": "Par20"}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 50, "text_sha256": "ef3c37a398cc33c2cac08d4fc06ef96648c5fcda5ce3de26387b1afb609af2bf", "xml_element_id": null}] plain_language: The HADHA 350/383/406 triple mutant remained susceptible to Dlat-induced acetylation in HEK293 cells. sample_size: 4 per group
    Complete structured claim and evidence

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