{"id":"dabd50dd-7a56-5dc4-b39a-b8320426c83c","stable_key":"d71929ae-ed38-52ed-b512-f92b9b148b71:ss-apt2-binding","predicate":"has_contextual_experimental_result","statement":"Surface plasmon resonance reported solasonine binding to recombinant APT2, KD 2.982 micromolar.","claim_class":"observational","status":"source_derived_draft","evidence_grade":"ungraded","direction":"neutral","is_public":true,"mechanism_event_id":"f00e961b-0025-50e0-917a-a4d1d7047ac2","mechanism_event_label":"ss-apt2-binding","subject":{"id":"6410ac1a-e95f-550f-955a-6725a3765ee3","slug":"solasonine","display_name":"Solasonine","entity_type_key":"small_molecule"},"object":{"id":"f2ffef5b-5457-50a8-b787-b8f24430f610","slug":"lypla2","display_name":"LYPLA2","entity_type_key":"protein"},"evidence_count":1,"mechanism_event":{"id":"f00e961b-0025-50e0-917a-a4d1d7047ac2","stable_key":"d71929ae-ed38-52ed-b512-f92b9b148b71:ss-apt2-binding","event_type":"experimental_result","label":"ss-apt2-binding","description":"Surface plasmon resonance reported solasonine binding to recombinant APT2, KD 2.982 micromolar.","status":"provisional","compartment":null,"participants":[{"entity":{"id":"6410ac1a-e95f-550f-955a-6725a3765ee3","slug":"solasonine","display_name":"Solasonine","entity_type_key":"small_molecule"},"role":"subject","stoichiometry":null,"state_label":"","sequence_order":0,"notes":""},{"entity":{"id":"f2ffef5b-5457-50a8-b787-b8f24430f610","slug":"lypla2","display_name":"LYPLA2","entity_type_key":"protein"},"role":"target","stoichiometry":null,"state_label":"","sequence_order":1,"notes":""}]},"contexts":[{"dimension":"experimental_model","value_text":"Recombinant human APT2 SPR; supporting cellular CETSA in NOZ/GBC-SD","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"exposure","value_text":"SPR binding concentration series; cellular CETSA used 25 micromolar solasonine. Binding does not specify catalytic inhibition.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"Human cancer-cell experiments; no clinical or dietary inference. Solasonine exposure is not equivalent to APT2 depletion, ML349, or sulforaphane. Mutant rescue does not by itself establish selectivity or normal baseline mutant function. Figure 5C calls this APT2 activity, but Methods 2.17 describes an anti-LYPLA2 ELISA with mass-concentration standards and an HRP/TMB readout from cell supernatants. No direct APT2 substrate-turnover assay is described there. The result is retained as an author-labelled activity proxy, not established catalytic inhibition. This methodological qualification does not invalidate the separately reported binding or cellular observations.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"organism","value_text":"Human","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_locator","value_text":"Figure 5J and Methods 2.20; CETSA Figure 5F-G.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"https://doi.org/10.1002/ptr.70245","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"c5b3f190-96ef-5c0a-b2ce-43c39e19ec35","evidence_kind":"source_excerpt","locator":"Lines 60-66","start_line":60,"end_line":66,"excerpt":"Surface plasmon resonance reported solasonine binding to recombinant APT2, KD 2.982 micromolar.\nprimary_references: https://doi.org/10.1002/ptr.70245\nprimary_locator: Figure 5J and Methods 2.20; CETSA Figure 5F-G.\norganism: Human\nexperimental_model: Recombinant human APT2 SPR; supporting cellular CETSA in NOZ/GBC-SD\nexposure: SPR binding concentration series; cellular CETSA used 25 micromolar solasonine. Binding does not specify catalytic inhibition.\nlimitations: Human cancer-cell experiments; no clinical or dietary inference. Solasonine exposure is not equivalent to APT2 depletion, ML349, or sulforaphane. Mutant rescue does not by itself establish selectivity or normal baseline mutant function. Figure 5C calls this APT2 activity, but Methods 2.17 describes an anti-LYPLA2 ELISA with mass-concentration standards and an HRP/TMB readout from cell supernatants. No direct APT2 substrate-turnover assay is described there. The result is retained as an author-labelled activity proxy, not established catalytic inhibition. This methodological qualification does not invalidate the separately reported binding or cellular observations.","model_system":"Recombinant human APT2 SPR; supporting cellular CETSA in NOZ/GBC-SD","directness":"reported_statement","verification_status":"source_derived_draft","notes":"Curator paraphrase, not a publisher quotation. Methodological inference is explicitly identified.","relationship":"supports","weight":1.0,"link_notes":"","source":{"id":"15a55d0b-bd44-54e4-9080-5526d1a9744d","stable_key":"import-d71929ae-ed38-52ed-b512-f92b9b148b71","title":"APT2, STAT3 and GPX4: opposing branches and assay qualification","document_type":"imported_text","citation_label":"Primary observations: 10.1038/s41467-025-56344-5 and 10.1002/ptr.70245; selected full-text review 2026-09-20.","file_path":"","sha256":"6fd94803c436074e7b2c15e9a817e751c3d95f6fe1d35a4af63ab641a8f33fe0","revision_id":"d59d5472-18d2-5feb-bc2e-529ceda00956","review_status":"unverified_draft","notes":""}}],"relations":[],"conflicts":[],"corrections":[],"research":null}