Component

TBK1 palmitoylation in mouse cells

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

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. LYPLA2 knockout prevented the reported stimulus-associated decline in TBK1 palmitoylation.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    experimental_model
    Mouse RAW 264.7; wild-type versus Lypla2 knockout
    exposure
    Plasmodium gDNA stimulation for 12 hours; concentration unresolved in this extraction.
    limitations
    Positive denotes preservation relative to stimulated wild-type, not an unqualified increase above resting baseline. No GPX4 endpoint.
    organism
    Mouse
    primary_locator
    Figure 3c; ABE and immunoblot.
    primary_references
    https://doi.org/10.1038/s41467-025-65081-8
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    MAVS inhibitor nulls and APT2-TBK1 immune feedback · lines 78–84

    Selected primary observations: 10.1073/pnas.2403392121; 10.1038/s41467-025-65081-8. · supports · Mouse RAW 264.7; wild-type versus Lypla2 knockout · source_derived_draft · unverified_draft

    LYPLA2 knockout prevented the reported stimulus-associated decline in TBK1 palmitoylation. primary_references: https://doi.org/10.1038/s41467-025-65081-8 primary_locator: Figure 3c; ABE and immunoblot. organism: Mouse experimental_model: Mouse RAW 264.7; wild-type versus Lypla2 knockout exposure: Plasmodium gDNA stimulation for 12 hours; concentration unresolved in this extraction. limitations: Positive denotes preservation relative to stimulated wild-type, not an unqualified increase above resting baseline. No GPX4 endpoint.
    Complete structured claim and evidence
  2. ML349 increased TBK1 palmitoylation in mouse peritoneal macrophages.

    Experimental context and source evidence
    experimental_model
    Mouse peritoneal exudate macrophages
    exposure
    ML349 concentration series for 12 hours; individual concentrations not transcribed from figure.
    limitations
    Concentration-response result; ABE is an S-acylation assay. No GPX4 endpoint in this experiment.
    organism
    Mouse
    primary_locator
    Figure 3b; ABE and immunoblot.
    primary_references
    https://doi.org/10.1038/s41467-025-65081-8

    MAVS inhibitor nulls and APT2-TBK1 immune feedback · lines 69–75

    Selected primary observations: 10.1073/pnas.2403392121; 10.1038/s41467-025-65081-8. · supports · Mouse peritoneal exudate macrophages · source_derived_draft · unverified_draft

    ML349 increased TBK1 palmitoylation in mouse peritoneal macrophages. primary_references: https://doi.org/10.1038/s41467-025-65081-8 primary_locator: Figure 3b; ABE and immunoblot. organism: Mouse experimental_model: Mouse peritoneal exudate macrophages exposure: ML349 concentration series for 12 hours; individual concentrations not transcribed from figure. limitations: Concentration-response result; ABE is an S-acylation assay. No GPX4 endpoint in this experiment.
    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