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(2010). https://pubmed.ncbi.nlm.nih.gov/19884324/ DOI: 10.1124/dmd.109.030445","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"FMN-dependent electron transfer","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"trigger_kind","value_text":"machinery_impairment","comparator":null,"unit":null,"notes":"Imported condition classification; unverified.","entity":null}],"evidence":[{"id":"6e2b59e3-adfd-5404-b164-d0c950c1c6c0","evidence_kind":"source_excerpt","locator":"Lines 285-296","start_line":285,"end_line":296,"excerpt":"### dim-por-fmn-rescue\nAdded FMN restored CYP1A2 ethoxyresorufin activity in POR Y181D membranes to 37% of the wild-type system.\nCondition category: machinery_impairment\nnutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: A specific cofactor-binding defect could be partly rescued in the assay.\norganism: Human POR Y181D and human CYP1A2 in engineered systems\ntissue_or_cell_type: FMN-dependent electron transfer\nexperimental_model: Recombinant protein and engineered bacterial coexpression\nlimitations: In-vitro rescue of one mutant; not a dietary-riboflavin deficiency experiment or evidence that FMN reverses a DIM-drug interaction.\nexposure: POR mutation and added FMN\nevidence_span: {\"source_cache\": \"artifacts/dim-research/19884324.abstract.txt\", \"locator\": \"Primary indexed abstract; zero-based, end-exclusive Unicode character offsets\", \"file_sha256\": \"3f702cc9af1528241d8572b8bcafc23dacb5ed3cacf6bb77403e8aa40d21a214\", \"start_char\": 0, \"end_char\": 1738, \"text_sha256\": \"3f702cc9af1528241d8572b8bcafc23dacb5ed3cacf6bb77403e8aa40d21a214\"}\n[dim-p19884324] Human cytochrome P450 oxidoreductase deficiency caused by the Y181D mutation: molecular consequences and rescue of defect. 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