{"id":"79eb7cac-5344-5001-932b-0e50cbfe23a6","stable_key":"31b1baa4-4113-5541-b9e7-fe44a5253a07:compound-c-mid1-null","predicate":"no_detected_change_in_recorded_experiment","statement":"Compound C did not alter MID1IP1 expression in the tested HepG2 comparison.","claim_class":"observational","status":"source_derived_draft","evidence_grade":"ungraded","direction":"neutral","is_public":true,"mechanism_event_id":"5fed3ff8-86a8-5e77-a2f1-f56f5ad11ac7","mechanism_event_label":"Compound C did not alter MID1IP1 expression in the tested HepG2 comparison.","subject":{"id":"599ac23b-aba7-58a7-89e3-254ebb938852","slug":"compound-c-ampk-inhibitor","display_name":"Compound C AMPK inhibitor","entity_type_key":"drug"},"object":{"id":"15810693-dac5-5c46-b80b-d57124cd2aae","slug":"human-mid1ip1","display_name":"Human MID1 interacting protein 1 / MID1IP1","entity_type_key":"protein"},"evidence_count":1,"mechanism_event":{"id":"5fed3ff8-86a8-5e77-a2f1-f56f5ad11ac7","stable_key":"31b1baa4-4113-5541-b9e7-fe44a5253a07:compound-c-mid1-null-event","event_type":"experimental_observation","label":"Compound C did not alter MID1IP1 expression in the tested HepG2 comparison.","description":"**The lipid study contains a useful null result.** Depleting MID1IP1 by siRNA in HepG2 cells reduced SREBP-1c and FAS expression and increased AMPK/ACC phosphorylation. In mouse AML-12 cells, MID1IP1 overexpression attenuated AMPK phosphorylation associated with 80 µM shikimic acid. Conversely, compound C did not alter MID1IP1 expression in the tested HepG2 comparison. This limits a simple claim that AMPK inhibition must reverse every MID1IP1 response. The source tested 10–160 µM SA in viability assays; MTT could fall to about 70% of control at the highest concentration, so reduced lipid staining must not be interpreted without viability context. [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":"599ac23b-aba7-58a7-89e3-254ebb938852","slug":"compound-c-ampk-inhibitor","display_name":"Compound C AMPK inhibitor","entity_type_key":"drug"},"role":"tested factor","stoichiometry":null,"state_label":"Compound C in the recorded comparison","sequence_order":0,"notes":""},{"entity":{"id":"15810693-dac5-5c46-b80b-d57124cd2aae","slug":"human-mid1ip1","display_name":"Human MID1 interacting protein 1 / MID1IP1","entity_type_key":"protein"},"role":"measured outcome","stoichiometry":null,"state_label":"no_detected_change","sequence_order":1,"notes":""}]},"contexts":[{"dimension":"evidence_access","value_text":"Primary full text retrieved; relevant methods/results/figures reviewed. 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In mouse AML-12 cells, MID1IP1 overexpression attenuated AMPK phosphorylation associated with 80 µM shikimic acid. Conversely, compound C did not alter MID1IP1 expression in the tested HepG2 comparison. This limits a simple claim that AMPK inhibition must reverse every MID1IP1 response. The source tested 10–160 µM SA in viability assays; MTT could fall to about 70% of control at the highest concentration, so reduced lipid staining must not be interpreted without viability context. [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 pharmacological signaling experiment.","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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