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.

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.

Recorded relationships

What acts on it

  1. The PI3K inhibitor ly294002 reduced the SA-associated mTOR phosphorylation increase.

    LY294002 → Rat OPC mTOR phosphorylation source_derived_draftungraded
    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 evidence
  2. SA increased mTOR phosphorylation in cultured rat OPCs.

    Shikimic acid → Rat OPC mTOR phosphorylation source_derived_draftungraded
    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 evidence
  3. The PI3K inhibitor wortmannin reduced the SA-associated mTOR phosphorylation increase.

    Wortmannin → Rat OPC mTOR phosphorylation source_derived_draftungraded
    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

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.