Component
Rat OPC mTOR phosphorylation
3 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
The PI3K inhibitor ly294002 reduced the SA-associated mTOR phosphorylation increase.
Experimental context and source evidence
- evidence_access
- Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
- experimental_condition
- SA without the inhibitor present · LY294002 Condition belongs to the full experimental contrast; do not separate a joint intervention.
- experimental_condition
- SA without the inhibitor present · Shikimic acid Condition belongs to the full experimental contrast; do not separate a joint intervention.
- experimental_contrast
- {"intervention": "ly294002 plus SA", "comparator": "SA without the inhibitor", "endpoint": "The PI3K inhibitor ly294002 reduced the SA-associated mTOR phosphorylation increase.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "ly294002", "state": "present"}, {"entity_slug": "shikimic-acid", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
- experimental_model
- Primary rat OPC joint pharmacological perturbation.
- interpretation_status
- Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
- limitations
- Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
- plain_language
- The PI3K inhibitor ly294002 reduced the SA-associated mTOR phosphorylation increase.
- primary_references
- Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice. | 2019 | DOI 10.1007/s12264-018-0322-7 | PMID 30684125 | https://pubmed.ncbi.nlm.nih.gov/30684125/ | https://doi.org/10.1007/s12264-018-0322-7 | https://pmc.ncbi.nlm.nih.gov/articles/PMC6527532/
- source_locator
- Reviewed reference lines 71-71; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 71–71
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Primary rat OPC joint pharmacological perturbation. · source_derived_draft · unverified_draft
**Perturbations expose a conditional signaling route.** In those rat precursor cultures, rapamycin blocked the shikimic-acid-associated rise in MBP, while the MEK inhibitor U0126 did not abolish it. PI3K inhibitors wortmannin and LY294002 reduced the elevated mTOR-phosphorylation readout toward control. These are joint experimental contrasts supporting pathway dependence; they do not establish that shikimic acid binds mTOR or that all MEK activity is irrelevant. [Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice.](https://pubmed.ncbi.nlm.nih.gov/30684125/)
Complete structured claim and evidenceSA increased mTOR phosphorylation in cultured rat OPCs.
Experimental context and source evidence
- evidence_access
- Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
- experimental_contrast
- {"intervention": "SA 100 µg/mL", "comparator": "Vehicle", "endpoint": "SA increased mTOR phosphorylation in cultured rat OPCs.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
- experimental_model
- Primary rat OPC signaling assay.
- interpretation_status
- Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
- limitations
- Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
- plain_language
- SA increased mTOR phosphorylation in cultured rat OPCs.
- primary_references
- Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice. | 2019 | DOI 10.1007/s12264-018-0322-7 | PMID 30684125 | https://pubmed.ncbi.nlm.nih.gov/30684125/ | https://doi.org/10.1007/s12264-018-0322-7 | https://pmc.ncbi.nlm.nih.gov/articles/PMC6527532/
- source_locator
- Reviewed reference lines 71-71; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 71–71
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Primary rat OPC signaling assay. · source_derived_draft · unverified_draft
**Perturbations expose a conditional signaling route.** In those rat precursor cultures, rapamycin blocked the shikimic-acid-associated rise in MBP, while the MEK inhibitor U0126 did not abolish it. PI3K inhibitors wortmannin and LY294002 reduced the elevated mTOR-phosphorylation readout toward control. These are joint experimental contrasts supporting pathway dependence; they do not establish that shikimic acid binds mTOR or that all MEK activity is irrelevant. [Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice.](https://pubmed.ncbi.nlm.nih.gov/30684125/)
Complete structured claim and evidenceThe PI3K inhibitor wortmannin reduced the SA-associated mTOR phosphorylation increase.
Experimental context and source evidence
- evidence_access
- Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
- experimental_condition
- SA without the inhibitor present · Wortmannin Condition belongs to the full experimental contrast; do not separate a joint intervention.
- experimental_condition
- SA without the inhibitor present · Shikimic acid Condition belongs to the full experimental contrast; do not separate a joint intervention.
- experimental_contrast
- {"intervention": "wortmannin plus SA", "comparator": "SA without the inhibitor", "endpoint": "The PI3K inhibitor wortmannin reduced the SA-associated mTOR phosphorylation increase.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "wortmannin", "state": "present"}, {"entity_slug": "shikimic-acid", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
- experimental_model
- Primary rat OPC joint pharmacological perturbation.
- interpretation_status
- Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
- limitations
- Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
- plain_language
- The PI3K inhibitor wortmannin reduced the SA-associated mTOR phosphorylation increase.
- primary_references
- Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice. | 2019 | DOI 10.1007/s12264-018-0322-7 | PMID 30684125 | https://pubmed.ncbi.nlm.nih.gov/30684125/ | https://doi.org/10.1007/s12264-018-0322-7 | https://pmc.ncbi.nlm.nih.gov/articles/PMC6527532/
- source_locator
- Reviewed reference lines 71-71; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 71–71
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Primary rat OPC joint pharmacological perturbation. · source_derived_draft · unverified_draft
**Perturbations expose a conditional signaling route.** In those rat precursor cultures, rapamycin blocked the shikimic-acid-associated rise in MBP, while the MEK inhibitor U0126 did not abolish it. PI3K inhibitors wortmannin and LY294002 reduced the elevated mTOR-phosphorylation readout toward control. These are joint experimental contrasts supporting pathway dependence; they do not establish that shikimic acid binds mTOR or that all MEK activity is irrelevant. [Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice.](https://pubmed.ncbi.nlm.nih.gov/30684125/)
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.