Component

Mouse dihydrolipoyl acetyltransferase / Dlat

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

5 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. The authors fitted a HADHA-substrate response and reported an apparent Km interval of 1.553–2.425 µM.

    Mouse dihydrolipoyl acetyltransferase / Dlat → HADHA experimental construct, species unresolved 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-assay-construct
    evidence_location
    Figure 6K, fluorescence-density response versus HADHA concentration
    experimental_model
    Recombinant-protein acetylation assay
    exposure
    mouse-dlat
    limitations
    Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. Figure labels and reaction-rate calibration are insufficient for a transferable catalytic constant. Preserve as an author-reported apparent fit; do not use as a validated in-cell parameter.
    organism
    Recombinant mouse Dlat; HADHA construct sequence species unresolved in reviewed methods
    plain_language
    The authors fitted a HADHA-substrate response and reported an apparent Km interval of 1.553–2.425 µM.
    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
    reported_parameter
    Apparent Km 1.553–2.425 µM; not independently refitted
    tissue_or_cell_type
    Purified-protein reaction

    DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 88–103

    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

    The authors fitted a HADHA-substrate response and reported an apparent Km interval of 1.553–2.425 µM. 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 reported_parameter: Apparent Km 1.553–2.425 µM; not independently refitted primary_references: https://doi.org/10.1038/s41467-026-70703-w access_level: full_text_and_supplement_review evidence_location: Figure 6K, fluorescence-density response versus HADHA concentration endpoint: hadha-assay-construct exposure: mouse-dlat limitations: Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. Figure labels and reaction-rate calibration are insufficient for a transferable catalytic constant. Preserve as an author-reported apparent fit; do not use as a validated in-cell parameter. 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: The authors fitted a HADHA-substrate response and reported an apparent Km interval of 1.553–2.425 µM.
    Complete structured claim and evidence

  2. Purified mouse Dlat increased the acetyl-lysine signal on recombinant HADHA when acetyl-CoA was present.

    Mouse dihydrolipoyl acetyltransferase / Dlat → HADHA experimental construct, species unresolved 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-assay-construct
    evidence_location
    Recombinant proteins and acetyl-lysine immunoblot; Figure 6J
    experimental_model
    Recombinant-protein acetylation assay
    exposure
    mouse-dlat
    limitations
    Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. Reported acetyltransferase interpretation; do not substitute tissue association for this biochemical evidence.
    organism
    Recombinant mouse Dlat; HADHA construct sequence species unresolved in reviewed methods
    plain_language
    Purified mouse Dlat increased the acetyl-lysine signal on recombinant HADHA when acetyl-CoA was present.
    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 52–67

    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

    Purified mouse Dlat increased the acetyl-lysine signal on recombinant HADHA when acetyl-CoA was present. 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: Recombinant proteins and acetyl-lysine immunoblot; Figure 6J endpoint: hadha-assay-construct exposure: mouse-dlat limitations: Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. Reported acetyltransferase interpretation; do not substitute tissue association for this biochemical evidence. 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: Purified mouse Dlat increased the acetyl-lysine signal on recombinant HADHA when acetyl-CoA was present. sample_size: 4 biological replicates
    Complete structured claim and evidence

  3. Mouse cardiac Dlat and HADHA co-immunoprecipitated; their association was stronger in the HFpEF model.

    Mouse dihydrolipoyl acetyltransferase / Dlat → Mouse mitochondrial trifunctional protein alpha subunit / Hadha source_derived_draftungraded
    Experimental context and source evidence
    access_level
    full_text_and_supplement_review
    compartment
    Cardiac tissue / mitochondria
    dose
    Two-hit model: 60% fat-calorie diet and L-NAME 0.5 g/L drinking water; vector dose not reported in reviewed text
    duration
    Two-hit protocol 15 weeks. Transgenic age/induction wording differs across passages; do not infer one exact interval
    endpoint
    mouse-hadha
    evidence_location
    Reciprocal co-immunoprecipitation; Figure 6D/E/H
    experimental_model
    Mouse two-hit HFpEF model: 60% fat-calorie diet plus L-NAME 0.5 g/L drinking water; additional intervention as stated
    exposure
    mouse-dlat
    limitations
    Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. Co-immunoprecipitation establishes association, not by itself direct binding or acetyl transfer.
    organism
    Mus musculus
    plain_language
    Mouse cardiac Dlat and HADHA co-immunoprecipitated; their association was stronger in the HFpEF model.
    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
    6 per group
    tissue_or_cell_type
    Cardiac tissue and cardiomyocytes

    DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 16–31

    AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Mouse two-hit HFpEF model: 60% fat-calorie diet plus L-NAME 0.5 g/L drinking water; additional intervention as stated · source_derived_draft · unverified_draft

    Mouse cardiac Dlat and HADHA co-immunoprecipitated; their association was stronger in the HFpEF model. organism: Mus musculus tissue_or_cell_type: Cardiac tissue and cardiomyocytes experimental_model: Mouse two-hit HFpEF model: 60% fat-calorie diet plus L-NAME 0.5 g/L drinking water; additional intervention as stated compartment: Cardiac tissue / mitochondria dose: Two-hit model: 60% fat-calorie diet and L-NAME 0.5 g/L drinking water; vector dose not reported in reviewed text duration: Two-hit protocol 15 weeks. Transgenic age/induction wording differs across passages; do not infer one exact interval primary_references: https://doi.org/10.1038/s41467-026-70703-w access_level: full_text_and_supplement_review evidence_location: Reciprocal co-immunoprecipitation; Figure 6D/E/H endpoint: mouse-hadha exposure: mouse-dlat limitations: Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. Co-immunoprecipitation establishes association, not by itself direct binding or acetyl transfer. 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: Mouse cardiac Dlat and HADHA co-immunoprecipitated; their association was stronger in the HFpEF model. sample_size: 6 per group
    Complete structured claim and evidence

Where it participates (unsigned role)

  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. 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

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.

    Evidence, AI assistance and curation standards