{"id":"d232534a-3b46-519a-8bc0-f5dad893a4ec","stable_key":"708c252b-0aef-5cec-95bf-99d19578214c:apt2-kd-stat3-nuclear","predicate":"has_contextual_experimental_result","statement":"APT2 knockdown reduced nuclear p-STAT3 in the HEK293T fractionation experiment.","claim_class":"observational","status":"source_derived_draft","evidence_grade":"ungraded","direction":"negative","is_public":true,"mechanism_event_id":"19f08d33-098b-5087-baa3-61b20c877879","mechanism_event_label":"apt2-kd-stat3-nuclear","subject":{"id":"3e4003ce-0ea9-5e6c-9c66-f02e69066754","slug":"human-apt2-knockdown-hek293t","display_name":"Human APT2/LYPLA2 knockdown in HEK293T","entity_type_key":"protein_state"},"object":{"id":"af10d4a5-0fa6-5659-89a4-9e60af4b937b","slug":"human-nuclear-pstat3-abundance","display_name":"Nuclear phosphorylated STAT3 abundance in human cells","entity_type_key":"cellular_process"},"evidence_count":1,"mechanism_event":{"id":"19f08d33-098b-5087-baa3-61b20c877879","stable_key":"708c252b-0aef-5cec-95bf-99d19578214c:apt2-kd-stat3-nuclear","event_type":"experimental_result","label":"apt2-kd-stat3-nuclear","description":"APT2 knockdown reduced nuclear p-STAT3 in the HEK293T fractionation experiment.","status":"provisional","compartment":null,"participants":[{"entity":{"id":"3e4003ce-0ea9-5e6c-9c66-f02e69066754","slug":"human-apt2-knockdown-hek293t","display_name":"Human APT2/LYPLA2 knockdown in HEK293T","entity_type_key":"protein_state"},"role":"subject","stoichiometry":null,"state_label":"","sequence_order":0,"notes":""},{"entity":{"id":"af10d4a5-0fa6-5659-89a4-9e60af4b937b","slug":"human-nuclear-pstat3-abundance","display_name":"Nuclear phosphorylated STAT3 abundance in human cells","entity_type_key":"cellular_process"},"role":"target","stoichiometry":null,"state_label":"","sequence_order":1,"notes":""},{"entity":{"id":"f2ffef5b-5457-50a8-b787-b8f24430f610","slug":"lypla2","display_name":"LYPLA2","entity_type_key":"protein"},"role":"depleted protein","stoichiometry":null,"state_label":"","sequence_order":2,"notes":""},{"entity":{"id":"dc129d3d-aaa0-5511-9a60-3e3880b0eb0f","slug":"stat3","display_name":"STAT3","entity_type_key":"protein"},"role":"measured protein","stoichiometry":null,"state_label":"","sequence_order":3,"notes":""}]},"contexts":[{"dimension":"availability_state","value_text":"machinery_impairment","comparator":null,"unit":null,"notes":"Imported condition classification; unverified.","entity":null},{"dimension":"experimental_model","value_text":"Human HEK293T subcellular fractionation","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"exposure","value_text":"LYPLA2 siRNA; exact dose/duration for this panel unresolved.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"Reported cellular result, not a GPX4 time-course experiment. 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Overexpressed DHHC constructs in much of the study are mouse proteins; human constructs are explicitly identified only where confirmed. APT2 depletion, selective inhibitor exposure and sulforaphane are different interventions.","model_system":"Human HEK293T subcellular fractionation","directness":"reported_statement","verification_status":"source_derived_draft","notes":"Curator paraphrase of the specified primary result; not a publisher quotation.","relationship":"supports","weight":1.0,"link_notes":"","source":{"id":"01fc674f-07c6-58fd-b1e7-877478a4472e","stable_key":"import-708c252b-0aef-5cec-95bf-99d19578214c","title":"APT2-STAT3 cycling and a competing sulforaphane target route","document_type":"imported_text","citation_label":"Selected primary observations: 10.1038/s41586-020-2799-2 and 10.1038/s41388-020-1335-z.","file_path":"","sha256":"b1b245468dac7acc94a2fef690d994124b2bc4fc5f92135173cf5636af391395","revision_id":"d84b8419-69dd-50d9-b587-5627ed414591","review_status":"unverified_draft","notes":""}}],"relations":[],"conflicts":[],"corrections":[],"research":null}