Component
Neurite and axonal outgrowth against inhibitory substrate
Neurite and axonal outgrowth against inhibitory substrate. 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)
Ibuprofen activates peroxisome proliferator-activated receptor gamma in neuron-like PC12 and B104 cells, activation with traditional agonists mimics the RhoA-inhibiting properties of ibuprofen and promotes neurite elongation in primary neurons exposed to axonal growth inhibitors, small interfering RNA against the receptor blocks RhoA suppression by those agonists, and selective receptor inhibition prevents the effect of ibuprofen on RhoA activity and neurite growth, supporting an essential role for the receptor in coupling ibuprofen to RhoA inhibition.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/ibuprofen-research/20089905.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "77e2dbb010dcee44bd66645ec26cb844d7041ea4930f6373ae5dd6b10da37df3", "start_char": 0, "end_char": 1812, "text_sha256": "77e2dbb010dcee44bd66645ec26cb844d7041ea4930f6373ae5dd6b10da37df3"}
- experimental_model
- Neuron-like PC12 and B104 cells and primary cultured neurons with small interfering RNA knockdown
- exposure
- Ibuprofen with peroxisome proliferator-activated receptor gamma agonists, antagonists and knockdown
- limitations
- The knockdown and the selective antagonist together make the receptor requirement a test rather than a correlation. Cell lines and primary culture rather than an animal.
- nutrient_topic
- Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. · Ibuprofen
- organism
- Rat
- plain_language
- The drug reaches a growth-blocking switch in neurons through a fat-sensing receptor, not through prostaglandins.
- primary_references
- [ibu-p20089905] A molecular mechanism for ibuprofen-mediated RhoA inhibition in neurons. (2010). https://pubmed.ncbi.nlm.nih.gov/20089905/ DOI: 10.1523/jneurosci.5045-09.2010
- tissue_or_cell_type
- Neurons
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Neuron-like PC12 and B104 cells and primary cultured neurons with small interfering RNA knockdown · source_derived_draft · unverified_draft
### ibu-pparg-couples-to-rhoa Ibuprofen activates peroxisome proliferator-activated receptor gamma in neuron-like PC12 and B104 cells, activation with traditional agonists mimics the RhoA-inhibiting properties of ibuprofen and promotes neurite elongation in primary neurons exposed to axonal growth inhibitors, small interfering RNA against the receptor blocks RhoA suppression by those agonists, and selective receptor inhibition prevents the effect of ibuprofen on RhoA activity and neurite growth, supporting an essential role for the receptor in coupling ibuprofen to RhoA inhibition. Condition category: normal nutrient_topic: Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. plain_language: The drug reaches a growth-blocking switch in neurons through a fat-sensing receptor, not through prostaglandins. organism: Rat tissue_or_cell_type: Neurons experimental_model: Neuron-like PC12 and B104 cells and primary cultured neurons with small interfering RNA knockdown limitations: The knockdown and the selective antagonist together make the receptor requirement a test rather than a correlation. Cell lines and primary culture rather than an animal. exposure: Ibuprofen with peroxisome proliferator-activated receptor gamma agonists, antagonists and knockdown evidence_span: {"source_cache": "artifacts/ibuprofen-research/20089905.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "77e2dbb010dcee44bd66645ec26cb844d7041ea4930f6373ae5dd6b10da37df3", "start_char": 0, "end_char": 1812, "text_sha256": "77e2dbb010dcee44bd66645ec26cb844d7041ea4930f6373ae5dd6b10da37df3"} [ibu-p20089905] A molecular mechanism for ibuprofen-mediated RhoA inhibition in neurons. (2010). https://pubmed.ncbi.nlm.nih.gov/20089905/ DOI: 10.1523/jneurosci.5045-09.2010
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.