{"id":"fe562e39-7669-5119-9acd-b88e6ae8b3ec","stable_key":"0ad8610d-d575-5870-b7cd-763a9f750783:copper-cu-nrf2","predicate":"promotes","statement":"CuCl2 exposure promoted NRF2 nuclear translocation in the tested cancer cells.","claim_class":"mechanistic","status":"source_derived_draft","evidence_grade":"ungraded","direction":"context_dependent","is_public":true,"mechanism_event_id":"f51ad95b-b6e7-5e97-981f-5a27e6b3d009","mechanism_event_label":"A stress-response regulator moved to the cell’s DNA-containing compartment.","subject":{"id":"2a870bb5-05a0-5e51-a70c-a9a843a8b571","slug":"copper-ii","display_name":"Copper(II) ion","entity_type_key":"ion"},"object":{"id":"cdca3452-2c25-5228-bfac-a71e0a9cda21","slug":"nrf2-nuclear-translocation","display_name":"NRF2 nuclear translocation","entity_type_key":"cellular_process"},"evidence_count":1,"mechanism_event":{"id":"f51ad95b-b6e7-5e97-981f-5a27e6b3d009","stable_key":"0ad8610d-d575-5870-b7cd-763a9f750783:copper-cu-nrf2-event","event_type":"biochemical_relationship","label":"A stress-response regulator moved to the cell’s DNA-containing compartment.","description":"CuCl2 exposure promoted NRF2 nuclear translocation in the tested cancer cells.","status":"provisional","compartment":null,"participants":[{"entity":{"id":"dc472dd3-d383-567a-ab37-a9ec4e112df4","slug":"nfe2l2","display_name":"Human Nrf2 / NFE2L2","entity_type_key":"protein"},"role":"transcription factor","stoichiometry":null,"state_label":"","sequence_order":0,"notes":""},{"entity":{"id":"2a870bb5-05a0-5e51-a70c-a9a843a8b571","slug":"copper-ii","display_name":"Copper(II) ion","entity_type_key":"ion"},"role":"subject","stoichiometry":null,"state_label":"","sequence_order":1,"notes":""},{"entity":{"id":"cdca3452-2c25-5228-bfac-a71e0a9cda21","slug":"nrf2-nuclear-translocation","display_name":"NRF2 nuclear translocation","entity_type_key":"cellular_process"},"role":"target","stoichiometry":null,"state_label":"","sequence_order":2,"notes":""}]},"contexts":[{"dimension":"evidence_span","value_text":"{\"source_cache\": \"artifacts/copper-research/40944334.abstract.txt\", \"locator\": \"Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets\", \"file_sha256\": \"6df1716e8998546d22a1d96116e1bc35b1f7e24c94868ec5e441ada6a2be3e89\", \"start_char\": 0, \"end_char\": 1634, \"text_sha256\": \"6df1716e8998546d22a1d96116e1bc35b1f7e24c94868ec5e441ada6a2be3e89\"}","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_model","value_text":"Copper and iron exposure with transcription-factor knockdown","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"exposure","value_text":"CuCl2 or FeCl2 exposure; NFE2L2 or ATOX1 knockdown","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"One cancer-cell model. Expression changes do not prove increased glutathione synthesis, tumor progression, or a clinical nutrient interaction.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"nutrient_topic","value_text":"Copper research collection; topical membership is not evidence of a direct dietary effect.","comparator":null,"unit":null,"notes":"","entity":{"slug":"copper","display_name":"Copper","entity_type_key":"nutrient_element"}},{"dimension":"organism","value_text":"Human MDA-MB-231 breast cancer cells","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"plain_language","value_text":"A stress-response regulator moved to the cell’s DNA-containing compartment.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"[copper-p40944334] Copper induces cystine/glutamate antiporter SLC7A11 through the activation of Nrf2 and Atox1 pathways. (2025). https://pubmed.ncbi.nlm.nih.gov/40944334/ DOI: 10.1080/10715762.2025.2560847","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"Cellular amino-acid transport machinery","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"75e8f7db-da92-5d0c-b874-c79d41a30b86","evidence_kind":"source_excerpt","locator":"Lines 1287-1298","start_line":1287,"end_line":1298,"excerpt":"### copper-cu-nrf2\nCuCl2 exposure promoted NRF2 nuclear translocation in the tested cancer cells.\nCondition category: normal\nnutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: A stress-response regulator moved to the cell’s DNA-containing compartment.\norganism: Human MDA-MB-231 breast cancer cells\ntissue_or_cell_type: Cellular amino-acid transport machinery\nexperimental_model: Copper and iron exposure with transcription-factor knockdown\nlimitations: One cancer-cell model. Expression changes do not prove increased glutathione synthesis, tumor progression, or a clinical nutrient interaction.\nexposure: CuCl2 or FeCl2 exposure; NFE2L2 or ATOX1 knockdown\nevidence_span: {\"source_cache\": \"artifacts/copper-research/40944334.abstract.txt\", \"locator\": \"Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets\", \"file_sha256\": \"6df1716e8998546d22a1d96116e1bc35b1f7e24c94868ec5e441ada6a2be3e89\", \"start_char\": 0, \"end_char\": 1634, \"text_sha256\": \"6df1716e8998546d22a1d96116e1bc35b1f7e24c94868ec5e441ada6a2be3e89\"}\n[copper-p40944334] Copper induces cystine/glutamate antiporter SLC7A11 through the activation of Nrf2 and Atox1 pathways. 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