Component
Palmostatin B, experimental depalmitoylase inhibitor
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 it acts on
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
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.