Component

Rat myelin basic protein / Mbp

3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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. SA increased MBP-associated OPC differentiation after 72 hours.

    Shikimic acid → Rat myelin basic protein / Mbp 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": "Shikimic acid", "comparator": "Vehicle", "endpoint": "SA increased MBP-associated OPC differentiation after 72 hours.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Primary rat OPCs, 1–100 µg/mL; 100 µg/mL (about 574 µM) used for follow-up.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    Differentiation marker, not all-cell proliferation or human therapeutic exposure.
    plain_language
    SA increased MBP-associated OPC differentiation after 72 hours.
    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 69-69; exact primary location described in quoted passage where extracted.

    Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 69–69

    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 OPCs, 1–100 µg/mL; 100 µg/mL (about 574 µM) used for follow-up. · source_derived_draft · unverified_draft

    **Oligodendrocyte differentiation differs from proliferation.** In primary rat oligodendrocyte precursor cultures, shikimic acid at 1–100 µg/mL increased MBP-associated differentiation after 72 h, with 100 µg/mL used for subsequent experiments. That highest concentration is calculated as about 574 µM. BrdU incorporation and TUNEL readouts did not significantly change. Increased MBP and fewer NG2-positive cells therefore support maturation in this model, not universal stimulation of cell proliferation. [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. Rapamycin blocked the SA-associated MBP increase.

    Rapamycin / sirolimus → Rat myelin basic protein / Mbp 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 · Shikimic acid Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_condition
    SA without the inhibitor present · Rapamycin / sirolimus Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "rapamycin plus SA", "comparator": "SA without the inhibitor", "endpoint": "Rapamycin blocked the SA-associated MBP increase.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "rapamycin", "state": "present"}, {"entity_slug": "shikimic-acid", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Primary rat OPC joint exposure, 100 µg/mL SA.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    Persistence with U0126 is not a blanket null for MEK activity. Inhibitors do not identify the direct SA target.
    plain_language
    Rapamycin blocked the SA-associated MBP 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 exposure, 100 µg/mL SA. · 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 SA-associated MBP increase persisted in the presence of U0126.

    U0126 MEK-pathway inhibitor → Rat myelin basic protein / Mbp 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 · Shikimic acid Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_condition
    SA without the inhibitor present · U0126 MEK-pathway inhibitor Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "u0126 plus SA", "comparator": "SA without the inhibitor", "endpoint": "The SA-associated MBP increase persisted in the presence of U0126.", "effect_direction": "not_reported", "combination": "joint", "conditions": [{"entity_slug": "u0126", "state": "present"}, {"entity_slug": "shikimic-acid", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Primary rat OPC joint exposure, 100 µg/mL SA.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    Persistence with U0126 is not a blanket null for MEK activity. Inhibitors do not identify the direct SA target.
    plain_language
    The SA-associated MBP increase persisted in the presence of U0126.
    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 exposure, 100 µg/mL SA. · 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.