Component

Human mitochondrial antiviral-signaling protein / MAVS

5 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

Where it participates (unsigned role)

  1. Treatment with ML348 did not produce a reported increase in endogenous MAVS S-acylation in HEK293T.

    Experimental context and source evidence
    experimental_model
    Human HEK293T; endogenous MAVS; acyl-biotin exchange with hydroxylamine-minus controls
    exposure
    Inhibitor treatment; dose and duration unresolved; no RLR stimulation specified in S2C.
    limitations
    Null under the reported assay, not proof of no effect at other sites, durations or activation states. Figure S2C and its legend visually reviewed. Exact inhibitor concentrations/durations were not located in the main methods or S2 legend; no matched exposure comparison with the Molecular Cell 2024 study is established.
    organism
    Human
    primary_locator
    SI Appendix Figure S2C; main Results: MAVS Is S-Palmitoylated by ZDHHC7.
    primary_references
    https://doi.org/10.1073/pnas.2403392121

    MAVS inhibitor nulls and APT2-TBK1 immune feedback · lines 15–21

    Selected primary observations: 10.1073/pnas.2403392121; 10.1038/s41467-025-65081-8. · supports · Human HEK293T; endogenous MAVS; acyl-biotin exchange with hydroxylamine-minus controls · source_derived_draft · unverified_draft

    Treatment with ML348 did not produce a reported increase in endogenous MAVS S-acylation in HEK293T. primary_references: https://doi.org/10.1073/pnas.2403392121 primary_locator: SI Appendix Figure S2C; main Results: MAVS Is S-Palmitoylated by ZDHHC7. organism: Human experimental_model: Human HEK293T; endogenous MAVS; acyl-biotin exchange with hydroxylamine-minus controls exposure: Inhibitor treatment; dose and duration unresolved; no RLR stimulation specified in S2C. limitations: Null under the reported assay, not proof of no effect at other sites, durations or activation states. Figure S2C and its legend visually reviewed. Exact inhibitor concentrations/durations were not located in the main methods or S2 legend; no matched exposure comparison with the Molecular Cell 2024 study is established.
    Complete structured claim and evidence
  2. Treatment with ML349 did not produce a reported increase in endogenous MAVS S-acylation in HEK293T.

    Experimental context and source evidence
    experimental_model
    Human HEK293T; endogenous MAVS; acyl-biotin exchange with hydroxylamine-minus controls
    exposure
    Inhibitor treatment; dose and duration unresolved; no RLR stimulation specified in S2C.
    limitations
    Null under the reported assay, not proof of no effect at other sites, durations or activation states. Figure S2C and its legend visually reviewed. Exact inhibitor concentrations/durations were not located in the main methods or S2 legend; no matched exposure comparison with the Molecular Cell 2024 study is established.
    organism
    Human
    primary_locator
    SI Appendix Figure S2C; main Results: MAVS Is S-Palmitoylated by ZDHHC7.
    primary_references
    https://doi.org/10.1073/pnas.2403392121

    MAVS inhibitor nulls and APT2-TBK1 immune feedback · lines 6–12

    Selected primary observations: 10.1073/pnas.2403392121; 10.1038/s41467-025-65081-8. · supports · Human HEK293T; endogenous MAVS; acyl-biotin exchange with hydroxylamine-minus controls · source_derived_draft · unverified_draft

    Treatment with ML349 did not produce a reported increase in endogenous MAVS S-acylation in HEK293T. primary_references: https://doi.org/10.1073/pnas.2403392121 primary_locator: SI Appendix Figure S2C; main Results: MAVS Is S-Palmitoylated by ZDHHC7. organism: Human experimental_model: Human HEK293T; endogenous MAVS; acyl-biotin exchange with hydroxylamine-minus controls exposure: Inhibitor treatment; dose and duration unresolved; no RLR stimulation specified in S2C. limitations: Null under the reported assay, not proof of no effect at other sites, durations or activation states. Figure S2C and its legend visually reviewed. Exact inhibitor concentrations/durations were not located in the main methods or S2 legend; no matched exposure comparison with the Molecular Cell 2024 study is established.
    Complete structured claim and evidence
  3. Treatment with PALMOSTATIN-B did not produce a reported increase in endogenous MAVS S-acylation in HEK293T.

    Experimental context and source evidence
    experimental_model
    Human HEK293T; endogenous MAVS; acyl-biotin exchange with hydroxylamine-minus controls
    exposure
    Inhibitor treatment; dose and duration unresolved; no RLR stimulation specified in S2C.
    limitations
    Null under the reported assay, not proof of no effect at other sites, durations or activation states. Figure S2C and its legend visually reviewed. Exact inhibitor concentrations/durations were not located in the main methods or S2 legend; no matched exposure comparison with the Molecular Cell 2024 study is established.
    organism
    Human
    primary_locator
    SI Appendix Figure S2C; main Results: MAVS Is S-Palmitoylated by ZDHHC7.
    primary_references
    https://doi.org/10.1073/pnas.2403392121

    MAVS inhibitor nulls and APT2-TBK1 immune feedback · lines 24–30

    Selected primary observations: 10.1073/pnas.2403392121; 10.1038/s41467-025-65081-8. · supports · Human HEK293T; endogenous MAVS; acyl-biotin exchange with hydroxylamine-minus controls · source_derived_draft · unverified_draft

    Treatment with PALMOSTATIN-B did not produce a reported increase in endogenous MAVS S-acylation in HEK293T. primary_references: https://doi.org/10.1073/pnas.2403392121 primary_locator: SI Appendix Figure S2C; main Results: MAVS Is S-Palmitoylated by ZDHHC7. organism: Human experimental_model: Human HEK293T; endogenous MAVS; acyl-biotin exchange with hydroxylamine-minus controls exposure: Inhibitor treatment; dose and duration unresolved; no RLR stimulation specified in S2C. limitations: Null under the reported assay, not proof of no effect at other sites, durations or activation states. Figure S2C and its legend visually reviewed. Exact inhibitor concentrations/durations were not located in the main methods or S2 legend; no matched exposure comparison with the Molecular Cell 2024 study is established.
    Complete structured claim and evidence
  4. ZDHHC7 knockout decreased endogenous MAVS S-acylation in HEK293T.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    experimental_model
    Human HEK293T; endogenous proteins; acyl-biotin exchange
    exposure
    Genetic ZDHHC7 knockout.
    limitations
    Endogenous knockout is distinct from murine ZDHHC plasmid overexpression elsewhere in this paper. ABE measures S-acylation, not the abundance of a specified acyl chain.
    organism
    Human
    primary_locator
    Figure 1C; SI Figure S1E, n=5.
    primary_references
    https://doi.org/10.1073/pnas.2403392121
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    MAVS inhibitor nulls and APT2-TBK1 immune feedback · lines 33–39

    Selected primary observations: 10.1073/pnas.2403392121; 10.1038/s41467-025-65081-8. · supports · Human HEK293T; endogenous proteins; acyl-biotin exchange · source_derived_draft · unverified_draft

    ZDHHC7 knockout decreased endogenous MAVS S-acylation in HEK293T. primary_references: https://doi.org/10.1073/pnas.2403392121 primary_locator: Figure 1C; SI Figure S1E, n=5. organism: Human experimental_model: Human HEK293T; endogenous proteins; acyl-biotin exchange exposure: Genetic ZDHHC7 knockout. limitations: Endogenous knockout is distinct from murine ZDHHC plasmid overexpression elsewhere in this paper. ABE measures S-acylation, not the abundance of a specified acyl chain.
    Complete structured claim and evidence
  5. ZDHHC7 knockout reduced MAVS aggregation after poly(I:C) stimulation in HEK293T.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    experimental_model
    Human HEK293T; wild-type versus ZDHHC7 knockout
    exposure
    Poly(I:C) transfection, 2 micrograms/mL for 8 hours.
    limitations
    Activation-dependent result. Crude P5 includes other organelles; this observation alone does not quantify purified mitochondrial localization.
    organism
    Human
    primary_locator
    Figure 1K; SDD-AGE of crude mitochondrial P5.
    primary_references
    https://doi.org/10.1073/pnas.2403392121
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    MAVS inhibitor nulls and APT2-TBK1 immune feedback · lines 42–48

    Selected primary observations: 10.1073/pnas.2403392121; 10.1038/s41467-025-65081-8. · supports · Human HEK293T; wild-type versus ZDHHC7 knockout · source_derived_draft · unverified_draft

    ZDHHC7 knockout reduced MAVS aggregation after poly(I:C) stimulation in HEK293T. primary_references: https://doi.org/10.1073/pnas.2403392121 primary_locator: Figure 1K; SDD-AGE of crude mitochondrial P5. organism: Human experimental_model: Human HEK293T; wild-type versus ZDHHC7 knockout exposure: Poly(I:C) transfection, 2 micrograms/mL for 8 hours. limitations: Activation-dependent result. Crude P5 includes other organelles; this observation alone does not quantify purified mitochondrial localization.
    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.

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