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(2000). https://pubmed.ncbi.nlm.nih.gov/11099045/ DOI: 10.1038/35042597","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"Proximal renal tubule","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":"bcc98991-f891-5724-80ac-8d2aa24329fe","evidence_kind":"source_excerpt","locator":"Lines 692-703","start_line":692,"end_line":703,"excerpt":"### chloride-clc5-vitd-loss\nThe Clcn5-null model lost 25-hydroxyvitamin D3 in urine.\nCondition category: machinery_impairment\nnutrient_topic: Chloride research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: The transporter defect connects chloride machinery to vitamin D handling.\norganism: Mouse\ntissue_or_cell_type: Proximal renal tubule\nexperimental_model: Clcn5 knockout and uptake measurements\nlimitations: The PTH/vitamin-D/hypercalciuria explanation includes proposed downstream steps; do not treat every link as demonstrated.\nexposure: Clcn5 disruption\nevidence_span: {\"source_cache\": \"artifacts/chloride-research/11099045.abstract.txt\", \"locator\": \"Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets\", \"file_sha256\": \"4929ed9da0f3702bbd28bf679f79c2dfb13b4e81d23e44327b27bebdcf3a7cca\", \"start_char\": 0, \"end_char\": 1218, \"text_sha256\": \"4929ed9da0f3702bbd28bf679f79c2dfb13b4e81d23e44327b27bebdcf3a7cca\"}\n[chloride-p11099045] ClC-5 Cl- -channel disruption impairs endocytosis in a mouse model for Dent's disease. 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