Component
Mouse mitochondrial antiviral-signaling protein / MAVS
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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
Where it participates (unsigned role)
ML349 increased the reported IRF3 phosphorylation response despite MAVS knockout in stimulated RAW 264.7 cells.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- experimental_model
- Mouse RAW 264.7; Mavs knockout
- exposure
- ML349 10 micromolar for 12 hours, then freeze-thawed Plasmodium yoelii N67 infected red blood cells for 6 hours.
- limitations
- MAVS loss reduces the baseline response. TBK1 loss removes a central signaling node; failure of rescue supports dependence but does not alone prove direct ML349 binding to TBK1. Not a viral infection experiment.
- organism
- Mouse
- primary_locator
- Figure 4j and corresponding Results; IFN-I activation is assessed here by immunoblot, not secreted interferon measurement.
- 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 51–57
Selected primary observations: 10.1073/pnas.2403392121; 10.1038/s41467-025-65081-8. · supports · Mouse RAW 264.7; Mavs knockout · source_derived_draft · unverified_draft
ML349 increased the reported IRF3 phosphorylation response despite MAVS knockout in stimulated RAW 264.7 cells. primary_references: https://doi.org/10.1038/s41467-025-65081-8 primary_locator: Figure 4j and corresponding Results; IFN-I activation is assessed here by immunoblot, not secreted interferon measurement. organism: Mouse experimental_model: Mouse RAW 264.7; Mavs knockout exposure: ML349 10 micromolar for 12 hours, then freeze-thawed Plasmodium yoelii N67 infected red blood cells for 6 hours. limitations: MAVS loss reduces the baseline response. TBK1 loss removes a central signaling node; failure of rescue supports dependence but does not alone prove direct ML349 binding to TBK1. Not a viral infection experiment.
Complete structured claim and evidenceML349 failed to restore the reported IRF3 phosphorylation response in TBK1-knockout RAW 264.7 cells.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- experimental_model
- Mouse RAW 264.7; Tbk1 knockout
- exposure
- ML349 10 micromolar for 12 hours, then freeze-thawed Plasmodium yoelii N67 infected red blood cells for 6 hours.
- limitations
- MAVS loss reduces the baseline response. TBK1 loss removes a central signaling node; failure of rescue supports dependence but does not alone prove direct ML349 binding to TBK1. Not a viral infection experiment.
- organism
- Mouse
- primary_locator
- Figure 4j and corresponding Results; IFN-I activation is assessed here by immunoblot, not secreted interferon measurement.
- 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 60–66
Selected primary observations: 10.1073/pnas.2403392121; 10.1038/s41467-025-65081-8. · supports · Mouse RAW 264.7; Tbk1 knockout · source_derived_draft · unverified_draft
ML349 failed to restore the reported IRF3 phosphorylation response in TBK1-knockout RAW 264.7 cells. primary_references: https://doi.org/10.1038/s41467-025-65081-8 primary_locator: Figure 4j and corresponding Results; IFN-I activation is assessed here by immunoblot, not secreted interferon measurement. organism: Mouse experimental_model: Mouse RAW 264.7; Tbk1 knockout exposure: ML349 10 micromolar for 12 hours, then freeze-thawed Plasmodium yoelii N67 infected red blood cells for 6 hours. limitations: MAVS loss reduces the baseline response. TBK1 loss removes a central signaling node; failure of rescue supports dependence but does not alone prove direct ML349 binding to TBK1. Not a viral infection experiment.
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.