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(2010). https://pubmed.ncbi.nlm.nih.gov/20699218/ DOI: 10.1074/jbc.m110.143826","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"Intestinal epithelium","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"0dcebf34-797c-58a0-9b13-51ee3a033fff","evidence_kind":"source_excerpt","locator":"Lines 351-362","start_line":351,"end_line":362,"excerpt":"### copper-ctr1-intestinal-adaptation\nDietary copper limitation increased total and apically localized Ctr1 protein in mouse intestine.\nCondition category: normal\nnutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: The intestine increased an entry route when copper supply fell.\norganism: Mouse, rat and pig; human HEK293T cells for separate processing experiments\ntissue_or_cell_type: Intestinal epithelium\nexperimental_model: Intestinal immunolocalization and dietary copper limitation\nlimitations: Apical Ctr1 was observed in the examined mammalian preparations; membrane localization is model dependent and cannot be assigned universally to every human intestinal condition.\nexposure: Copper limitation in mice\nevidence_span: {\"source_cache\": \"artifacts/copper-research/20699218.abstract.txt\", \"locator\": \"Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets\", \"file_sha256\": \"c638594d4e707bb39a8f2e8c1fed15a42982e1dc4d525fda112d28281a853012\", \"start_char\": 0, \"end_char\": 1749, \"text_sha256\": \"c638594d4e707bb39a8f2e8c1fed15a42982e1dc4d525fda112d28281a853012\"}\n[copper-p20699218] Ctr1 is an apical copper transporter in mammalian intestinal epithelial cells in vivo that is controlled at the level of protein stability. 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