{"id":"893a5c47-11b3-58e8-95ca-ac3237e4cb7d","stable_key":"31b1baa4-4113-5541-b9e7-fe44a5253a07:human-sa-acc-phosphorylation","predicate":"increases_in_recorded_experiment","statement":"SA increased Human HepG2 ACC phosphorylation.","claim_class":"observational","status":"source_derived_draft","evidence_grade":"ungraded","direction":"positive","is_public":true,"mechanism_event_id":"ddee7c78-3d92-57e0-a9e8-d9529f3cfbe6","mechanism_event_label":"SA increased Human HepG2 ACC phosphorylation.","subject":{"id":"67ad4a8f-1bf6-59e5-90a6-97b7709024d3","slug":"shikimic-acid","display_name":"Shikimic acid","entity_type_key":"small_molecule"},"object":{"id":"172f86bb-c482-55ce-9eba-cb14cf22bb0e","slug":"human-sa-acc-phosphorylation","display_name":"Human HepG2 ACC phosphorylation","entity_type_key":"cellular_process"},"evidence_count":1,"mechanism_event":{"id":"ddee7c78-3d92-57e0-a9e8-d9529f3cfbe6","stable_key":"31b1baa4-4113-5541-b9e7-fe44a5253a07:human-sa-acc-phosphorylation-event","event_type":"experimental_observation","label":"SA increased Human HepG2 ACC phosphorylation.","description":"**Lipid accumulation studies identify responses, not direct inhibition.** In HepG2/Huh7 and 3T3-L1 experiments, shikimic acid was associated with lower lipid staining and altered lipogenic proteins, including lower MID1IP1, LXRα and SREBP-1c; AMPKα and ACC phosphorylation increased in the reported cell contexts. Genetic manipulation of MID1IP1 and compound-C experiments probed pathway involvement. These cultured-cell observations do not prove direct binding to MID1IP1, human fatty-liver efficacy, or that AMPK causes the triglyceride change in the separate mouse-feeding study. Individual cell-dose details remain in the original paper rather than being guessed. [Hypolipogenic Effect of Shikimic Acid Via Inhibition of MID1IP1 and Phosphorylation of AMPK/ACC.](https://pubmed.ncbi.nlm.nih.gov/30700011/)","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 treatment","sequence_order":0,"notes":""},{"entity":{"id":"172f86bb-c482-55ce-9eba-cb14cf22bb0e","slug":"human-sa-acc-phosphorylation","display_name":"Human HepG2 ACC phosphorylation","entity_type_key":"cellular_process"},"role":"measured outcome","stoichiometry":null,"state_label":"increase","sequence_order":1,"notes":""}]},"contexts":[{"dimension":"evidence_access","value_text":"Primary full text retrieved; relevant methods/results/figures reviewed. 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Genetic manipulation of MID1IP1 and compound-C experiments probed pathway involvement. These cultured-cell observations do not prove direct binding to MID1IP1, human fatty-liver efficacy, or that AMPK causes the triglyceride change in the separate mouse-feeding study. Individual cell-dose details remain in the original paper rather than being guessed. [Hypolipogenic Effect of Shikimic Acid Via Inhibition of MID1IP1 and Phosphorylation of AMPK/ACC.](https://pubmed.ncbi.nlm.nih.gov/30700011/)","model_system":"Human HepG2 cell 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. 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