{"id":"e115c5f1-28cb-5de4-9e1e-1c8679cc869e","stable_key":"31b1baa4-4113-5541-b9e7-fe44a5253a07:opc-mtor","predicate":"increases_in_recorded_experiment","statement":"SA increased mTOR phosphorylation in cultured rat OPCs.","claim_class":"observational","status":"source_derived_draft","evidence_grade":"ungraded","direction":"positive","is_public":true,"mechanism_event_id":"06484d08-081d-5c1c-9b17-81923023fd78","mechanism_event_label":"SA increased mTOR phosphorylation in cultured rat OPCs.","subject":{"id":"67ad4a8f-1bf6-59e5-90a6-97b7709024d3","slug":"shikimic-acid","display_name":"Shikimic acid","entity_type_key":"small_molecule"},"object":{"id":"ba61bf20-8aff-5dab-a70f-19d7be965e84","slug":"rat-opc-mtor-phosphorylation","display_name":"Rat OPC mTOR phosphorylation","entity_type_key":"cellular_process"},"evidence_count":1,"mechanism_event":{"id":"06484d08-081d-5c1c-9b17-81923023fd78","stable_key":"31b1baa4-4113-5541-b9e7-fe44a5253a07:opc-mtor-event","event_type":"experimental_observation","label":"SA increased mTOR phosphorylation in cultured rat OPCs.","description":"**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/)","status":"provisional","compartment":null,"participants":[{"entity":{"id":"67ad4a8f-1bf6-59e5-90a6-97b7709024d3","slug":"shikimic-acid","display_name":"Shikimic acid","entity_type_key":"small_molecule"},"role":"tested factor","stoichiometry":null,"state_label":"SA 100 µg/mL","sequence_order":0,"notes":""},{"entity":{"id":"ba61bf20-8aff-5dab-a70f-19d7be965e84","slug":"rat-opc-mtor-phosphorylation","display_name":"Rat OPC mTOR phosphorylation","entity_type_key":"cellular_process"},"role":"measured outcome","stoichiometry":null,"state_label":"increase","sequence_order":1,"notes":""},{"entity":{"id":"7fca1403-41f3-5b05-a6fa-b19bd9f7d3fc","slug":"rat-mtor","display_name":"Rat mechanistic target of rapamycin / Mtor","entity_type_key":"protein"},"role":"measured protein","stoichiometry":null,"state_label":"","sequence_order":2,"notes":""}]},"contexts":[{"dimension":"evidence_access","value_text":"Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_contrast","value_text":"{\"intervention\": \"SA 100 µg/mL\", \"comparator\": \"Vehicle\", \"endpoint\": \"SA increased mTOR phosphorylation in cultured rat OPCs.\", \"effect_direction\": \"increase\", \"combination\": \"single\", \"conditions\": []}","comparator":null,"unit":null,"notes":"Explicit extracted experimental comparison; source-derived draft.","entity":null},{"dimension":"experimental_model","value_text":"Primary rat OPC signaling assay.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"interpretation_status","value_text":"Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"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.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"plain_language","value_text":"SA increased mTOR phosphorylation in cultured rat OPCs.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"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/","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"source_locator","value_text":"Reviewed reference lines 71-71; exact primary location described in quoted passage where extracted.","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"ff672d4a-e0a5-546f-9a53-daf21d02f784","evidence_kind":"source_excerpt","locator":"Lines 71-71","start_line":71,"end_line":71,"excerpt":"**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/)","model_system":"Primary rat OPC signaling assay.","directness":"reported_statement","verification_status":"source_derived_draft","notes":"Exact excerpt of the retained AI-assisted reviewed reference; primary sources are cited in primary_references and access scope is retained. Not a verbatim quotation from a primary paper.","relationship":"supports","weight":1.0,"link_notes":"","source":{"id":"e6ae59de-0369-5c2f-8262-57d91302671c","stable_key":"import-31b1baa4-4113-5541-b9e7-fe44a5253a07","title":"Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026)","document_type":"imported_text","citation_label":"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.","file_path":"","sha256":"95b1f9e9577661312d67f36e156d2e49326b207f296c1c0e801a5b007fd8e283","revision_id":"cd3237f1-131a-557d-84b5-7543259807b0","review_status":"unverified_draft","notes":""}}],"relations":[],"conflicts":[],"corrections":[],"research":null}