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(2021). https://pubmed.ncbi.nlm.nih.gov/33271457/ DOI: 10.1016/j.redox.2020.101800","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"HEK293T cells","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":"f88424cf-b351-5e88-bf0e-5146ec2899ae","evidence_kind":"source_excerpt","locator":"Lines 703-714","start_line":703,"end_line":714,"excerpt":"### mo-suox-h2s\nSUOX deficiency was accompanied by increased H2S steady-state levels without upregulation of the known H2S-producing pathways.\nCondition category: machinery_impairment\nnutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: The sulfur disturbance extends beyond sulfite, but its precise route remains unresolved.\norganism: Homo sapiens\ntissue_or_cell_type: HEK293T cells\nexperimental_model: CRISPR SUOX/GOT1/GOT2 perturbations and sulfur-metabolite assays\nlimitations: Cell-specific contributions; a higher concentration is not a direct measurement of pathway flux.\nexposure: Cysteine-sulfinate and H2S pathway experiments\nevidence_span: {\"source_cache\": \"artifacts/molybdenum-research/33271457.abstract.txt\", \"locator\": \"Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets\", \"file_sha256\": \"619710a31160db0927e01193e458277773ebe5e5423629e7dab58888ab6bc617\", \"start_char\": 0, \"end_char\": 1479, \"text_sha256\": \"619710a31160db0927e01193e458277773ebe5e5423629e7dab58888ab6bc617\"}\n[mo-p33271457] The role of glutamate oxaloacetate transaminases in sulfite biosynthesis and H<sub>2</sub>S metabolism. 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