Component
APT2 transcript abundance in mouse cells
1 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.
What acts on it
IFNAR deficiency reduced infected-red-cell-induced APT2 transcript expression in peritoneal macrophages.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- experimental_model
- Mouse wild-type versus Ifnar-deficient peritoneal exudate macrophages
- exposure
- Freeze-thawed Plasmodium yoelii N67 infected red blood cells at 0, 6, 12 and 24 hours (Figure 7d visually reviewed).
- limitations
- The manuscript calls the genotype Ifnar-deficient; this extraction does not assign a specific disrupted subunit allele. No specific IFNAR1 or IFNAR2 state link is inferred.
- organism
- Mouse
- primary_locator
- Figure 7d; RT-qPCR and Results.
- 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 96–102
Selected primary observations: 10.1073/pnas.2403392121; 10.1038/s41467-025-65081-8. · supports · Mouse wild-type versus Ifnar-deficient peritoneal exudate macrophages · source_derived_draft · unverified_draft
IFNAR deficiency reduced infected-red-cell-induced APT2 transcript expression in peritoneal macrophages. primary_references: https://doi.org/10.1038/s41467-025-65081-8 primary_locator: Figure 7d; RT-qPCR and Results. organism: Mouse experimental_model: Mouse wild-type versus Ifnar-deficient peritoneal exudate macrophages exposure: Freeze-thawed Plasmodium yoelii N67 infected red blood cells at 0, 6, 12 and 24 hours (Figure 7d visually reviewed). limitations: The manuscript calls the genotype Ifnar-deficient; this extraction does not assign a specific disrupted subunit allele. No specific IFNAR1 or IFNAR2 state link is inferred.
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.