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(2020). https://pubmed.ncbi.nlm.nih.gov/32084341/ DOI: 10.1016/j.cell.2020.01.023","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"Microbial glucosinolate activation","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":"c230cb8d-a605-5847-959a-0f5c3a60f0d2","evidence_kind":"source_excerpt","locator":"Lines 242-253","start_line":242,"end_line":253,"excerpt":"### sulforaphane-microbial-loss\nMice monoassociated with the BT2157-mutant strain had lower gastrointestinal isothiocyanate production.\nCondition category: machinery_impairment\nnutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: Losing microbial conversion capacity can reduce activation of the precursor.\norganism: B. thetaiotaomicron, engineered B. fragilis and monoassociated mice\ntissue_or_cell_type: Microbial glucosinolate activation\nexperimental_model: Bacterial genetics, purified-enzyme reconstitution and gnotobiotic mice\nlimitations: Microbial enzymes are distinct from plant myrosinase; general glucosinolate experiments do not prove every substrate follows identical kinetics.\nexposure: BT2159-BT2156 transfer; individual enzyme combinations and BT2157 mutant\nevidence_span: {\"source_cache\": \"artifacts/sulforaphane-research/32084341.abstract.txt\", \"locator\": \"Primary indexed abstract; zero-based, end-exclusive Unicode character offsets\", \"file_sha256\": \"08eaa102da24fdee1f16fa9376338c557ba4f3919adb1122f3e13d509a171293\", \"start_char\": 0, \"end_char\": 1031, \"text_sha256\": \"08eaa102da24fdee1f16fa9376338c557ba4f3919adb1122f3e13d509a171293\"}\n[sulforaphane-p32084341] A Metabolic Pathway for Activation of Dietary Glucosinolates by a Human Gut Symbiont. 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