Component
Phosphorylation and degradation of I-kappa-B-alpha
Phosphorylation and degradation of I-kappa-B-alpha. Species, exposure and limitations are retained in each linked claim.
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.
Where it participates (unsigned role)
The anti-inflammatory drugs sodium salicylate and aspirin inhibited activation of nuclear factor kappa B, an inhibition which prevented degradation of the inhibitor I-kappa-B so that nuclear factor kappa B was retained in the cytosol, and both also inhibited nuclear factor kappa B-dependent transcription from the immunoglobulin kappa enhancer and the human immunodeficiency virus long terminal repeat in transfected T cells.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/aspirin-research/8052854.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d1d488e1bc53706da4f733f3fecc2bb981c09c0aa2dccae2bac9fac1bb04cec1", "start_char": 0, "end_char": 737, "text_sha256": "d1d488e1bc53706da4f733f3fecc2bb981c09c0aa2dccae2bac9fac1bb04cec1"}
- experimental_model
- Electrophoretic mobility shift and reporter transcription assays in transfected T cells
- exposure
- Sodium salicylate and aspirin applied to nuclear factor kappa B activation
- limitations
- A cell-based mechanism recorded at the concentrations used in the assay, which are far above those reached by antiplatelet dosing. It does not distinguish the two compounds from one another.
- nutrient_topic
- Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. · Aspirin / acetylsalicylic acid
- organism
- Human cells
- plain_language
- Both compounds keep an inflammatory master switch locked out of the nucleus.
- primary_references
- [asa-p8052854] Inhibition of NF-kappa B by sodium salicylate and aspirin. (1994). https://pubmed.ncbi.nlm.nih.gov/8052854/ DOI: 10.1126/science.8052854
- tissue_or_cell_type
- T lymphocytes
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Electrophoretic mobility shift and reporter transcription assays in transfected T cells · source_derived_draft · unverified_draft
### asa-salicylate-blocks-nfkb The anti-inflammatory drugs sodium salicylate and aspirin inhibited activation of nuclear factor kappa B, an inhibition which prevented degradation of the inhibitor I-kappa-B so that nuclear factor kappa B was retained in the cytosol, and both also inhibited nuclear factor kappa B-dependent transcription from the immunoglobulin kappa enhancer and the human immunodeficiency virus long terminal repeat in transfected T cells. Condition category: normal nutrient_topic: Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. plain_language: Both compounds keep an inflammatory master switch locked out of the nucleus. organism: Human cells tissue_or_cell_type: T lymphocytes experimental_model: Electrophoretic mobility shift and reporter transcription assays in transfected T cells limitations: A cell-based mechanism recorded at the concentrations used in the assay, which are far above those reached by antiplatelet dosing. It does not distinguish the two compounds from one another. exposure: Sodium salicylate and aspirin applied to nuclear factor kappa B activation evidence_span: {"source_cache": "artifacts/aspirin-research/8052854.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d1d488e1bc53706da4f733f3fecc2bb981c09c0aa2dccae2bac9fac1bb04cec1", "start_char": 0, "end_char": 737, "text_sha256": "d1d488e1bc53706da4f733f3fecc2bb981c09c0aa2dccae2bac9fac1bb04cec1"} [asa-p8052854] Inhibition of NF-kappa B by sodium salicylate and aspirin. (1994). https://pubmed.ncbi.nlm.nih.gov/8052854/ DOI: 10.1126/science.8052854
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.