Component
NLRP3 in the myricetin ubiquitination assay; cell species unresolved in abstract
Context-specific entity; species, compartment and exposure are stated on each claim.
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.
What acts on it
Myricetin promoted ROS-independent NLRP3 ubiquitination in the reported inflammasome experiment.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Cellular inflammasome experiments with mouse sepsis/peritonitis validation.
- limitations
- Cell species and chain topology are unresolved in the accessed abstract; do not infer degradation or assign human protein identity.
- nutrient_topic
- Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
- plain_language
- A protein modification can change assembly of an inflammatory complex.
- primary_references
- Myricetin inhibits NLRP3 inflammasome activation via reduction of ROS-dependent ubiquitination of ASC and promotion of ROS-independent NLRP3 ubiquitination. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30594691/ · DOI 10.1016/j.taap.2018.12.019
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 620–626
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Cellular inflammasome experiments with mouse sepsis/peritonitis validation. · source_derived_draft · unverified_draft
## myricetin-nlrp3-ubiquitination A protein modification can change assembly of an inflammatory complex. Myricetin promoted ROS-independent NLRP3 ubiquitination in the reported inflammasome experiment. Model: Cellular inflammasome experiments with mouse sepsis/peritonitis validation. Limitations: Cell species and chain topology are unresolved in the accessed abstract; do not infer degradation or assign human protein identity. Evidence access: Primary abstract Myricetin inhibits NLRP3 inflammasome activation via reduction of ROS-dependent ubiquitination of ASC and promotion of ROS-independent NLRP3 ubiquitination. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30594691/ · DOI 10.1016/j.taap.2018.12.019
Complete structured claim and evidence
Where it participates (unsigned role)
Myricetin reduced ROS-dependent ASC ubiquitination and reduced ASC–NLRP3 interaction and ASC oligomerization.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Cellular inflammasome assembly assays.
- limitations
- No specific E3 ligase or ubiquitin-chain linkage established by the accessed abstract.
- nutrient_topic
- Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
- plain_language
- The two proteins did not show the same ubiquitination direction.
- primary_references
- Myricetin inhibits NLRP3 inflammasome activation via reduction of ROS-dependent ubiquitination of ASC and promotion of ROS-independent NLRP3 ubiquitination. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30594691/ · DOI 10.1016/j.taap.2018.12.019
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 628–634
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Cellular inflammasome assembly assays. · source_derived_draft · unverified_draft
## myricetin-asc-ubiquitination The two proteins did not show the same ubiquitination direction. Myricetin reduced ROS-dependent ASC ubiquitination and reduced ASC–NLRP3 interaction and ASC oligomerization. Model: Cellular inflammasome assembly assays. Limitations: No specific E3 ligase or ubiquitin-chain linkage established by the accessed abstract. Evidence access: Primary abstract Myricetin inhibits NLRP3 inflammasome activation via reduction of ROS-dependent ubiquitination of ASC and promotion of ROS-independent NLRP3 ubiquitination. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30594691/ · DOI 10.1016/j.taap.2018.12.019
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.