{"id":"ff02ad27-adac-5b78-b250-0238428de98e","stable_key":"066fc1e8-fefc-5be0-9905-938b10b89691:a39-kd-contacts","predicate":"has_contextual_experimental_effect","statement":"SLC25A39 knockdown increased ER-mitochondria contacts in HeLa MERBiT cells.","claim_class":"mechanistic","status":"source_derived_draft","evidence_grade":"ungraded","direction":"positive","is_public":true,"mechanism_event_id":"3ddcb7b0-3853-5dd2-aec4-89626790cf50","mechanism_event_label":"a39 kd contacts","subject":{"id":"543c9bd9-03a3-5a08-b1f7-08184225765e","slug":"human-a39-knockdown-hela","display_name":"SLC25A39 knockdown in HeLa cells","entity_type_key":"protein_state"},"object":{"id":"5748e8cb-31c9-58c3-8831-4132fe0b2757","slug":"human-mitochondria-er-contacts","display_name":"ER-mitochondria contacts in human cells","entity_type_key":"cellular_process"},"evidence_count":1,"mechanism_event":{"id":"3ddcb7b0-3853-5dd2-aec4-89626790cf50","stable_key":"066fc1e8-fefc-5be0-9905-938b10b89691:a39-kd-contacts","event_type":"experimental_result","label":"a39 kd contacts","description":"SLC25A39 knockdown increased ER-mitochondria contacts in HeLa MERBiT cells.","status":"provisional","compartment":null,"participants":[{"entity":{"id":"543c9bd9-03a3-5a08-b1f7-08184225765e","slug":"human-a39-knockdown-hela","display_name":"SLC25A39 knockdown in HeLa cells","entity_type_key":"protein_state"},"role":"subject","stoichiometry":null,"state_label":"","sequence_order":0,"notes":""},{"entity":{"id":"5748e8cb-31c9-58c3-8831-4132fe0b2757","slug":"human-mitochondria-er-contacts","display_name":"ER-mitochondria contacts in human cells","entity_type_key":"cellular_process"},"role":"target","stoichiometry":null,"state_label":"","sequence_order":1,"notes":""}]},"contexts":[{"dimension":"access_level","value_text":"selected_primary_main_text_and_legends; cached web/indexed passages, not complete supplement review","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"evidence_cache","value_text":"artifacts/discovery-research/round4-sources/contact-2025-indexed-passages.json; SHA256 9222f94099520a9b5e9ee8b7f30a1b4ae261735d37462b13d7ca3d0ecc8792d6","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_model","value_text":"HeLa; MERBiT reporter derivative where stated","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"exposure","value_text":"3-day siRNA exposure; MERBiT luminescence; dose unresolved","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"Selected primary main-text Results and figure legends reviewed; supplementary images not independently inspected. These two papers share authors and are not independent replication. They do not test whether SLC25A39-loss-induced contacts increase HMOX2-dependent iron delivery. ICP-MS measures total iron, not labile iron or transport flux. Contact loss affecting an outcome does not establish that increasing contacts increases it. Ubiquitination/activity readouts do not establish direct enzymatic activation or the outer-membrane iron transport machinery. No clinical or pulmonary-endothelial effect is inferred.","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 2f and Results: Induction of mitochondrial ROS","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"https://doi.org/10.1038/s41467-025-56666-4","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"ed49c578-a0fb-5aa2-aa60-025fba88dd01","evidence_kind":"source_excerpt","locator":"Lines 6-14","start_line":6,"end_line":14,"excerpt":"SLC25A39 knockdown increased ER-mitochondria contacts in HeLa MERBiT cells.\nprimary_references: https://doi.org/10.1038/s41467-025-56666-4\nprimary_locator: Figure 2f and Results: Induction of mitochondrial ROS\nevidence_cache: artifacts/discovery-research/round4-sources/contact-2025-indexed-passages.json; SHA256 9222f94099520a9b5e9ee8b7f30a1b4ae261735d37462b13d7ca3d0ecc8792d6\naccess_level: selected_primary_main_text_and_legends; cached web/indexed passages, not complete supplement review\norganism: Human\nexperimental_model: HeLa; MERBiT reporter derivative where stated\nexposure: 3-day siRNA exposure; MERBiT luminescence; dose unresolved\nlimitations: Selected primary main-text Results and figure legends reviewed; supplementary images not independently inspected. These two papers share authors and are not independent replication. They do not test whether SLC25A39-loss-induced contacts increase HMOX2-dependent iron delivery. ICP-MS measures total iron, not labile iron or transport flux. Contact loss affecting an outcome does not establish that increasing contacts increases it. Ubiquitination/activity readouts do not establish direct enzymatic activation or the outer-membrane iron transport machinery. No clinical or pulmonary-endothelial effect is inferred.","model_system":"Human HeLa cells","directness":"reported_statement","verification_status":"source_derived_draft","notes":"Authored paraphrase with primary location; not a publisher quotation.","relationship":"supports","weight":1.0,"link_notes":"","source":{"id":"e52836df-b22a-51c4-9ab4-6b258a554969","stable_key":"import-066fc1e8-fefc-5be0-9905-938b10b89691","title":"Glutathione, ER-mitochondria contacts, and iron: observed components","document_type":"imported_text","citation_label":"Targeted primary-literature curation, 2026-09-20. DOIs 10.1038/s41467-025-56666-4 and 10.1038/s41556-026-01974-0.","file_path":"","sha256":"381747aa54ebbd40dfc3d830264e0231a09c3e417ad896a591dffc10dcdc64f4","revision_id":"d679b06d-a889-5aba-b69b-f5c07d393c24","review_status":"unverified_draft","notes":""}}],"relations":[],"conflicts":[],"corrections":[],"research":null}