{"id":"c9f91703-7732-5a14-8035-1335c3e1159b","stable_key":"4df6a932-097e-563a-91fe-5dceec471ffd:chloride-clcnkb-potassium","predicate":"loss_of_function_lowers","statement":"Affected CLCNKB families had hypokalemia alongside salt wasting.","claim_class":"mechanistic","status":"source_derived_draft","evidence_grade":"ungraded","direction":"context_dependent","is_public":true,"mechanism_event_id":"9bffae70-e50a-5e6c-8e96-4af1aef22a19","mechanism_event_label":"Potassium deficiency can be downstream of defective chloride transport.","subject":{"id":"3f12ade5-3548-5748-a8d4-96ced78dd950","slug":"clcnkb","display_name":"Chloride channel ClC-Kb","entity_type_key":"protein"},"object":{"id":"bb23d568-e85f-5bdd-b264-92d73b8dce53","slug":"plasma-potassium-concentration","display_name":"Plasma potassium concentration","entity_type_key":"cellular_process"},"evidence_count":1,"mechanism_event":{"id":"9bffae70-e50a-5e6c-8e96-4af1aef22a19","stable_key":"4df6a932-097e-563a-91fe-5dceec471ffd:chloride-clcnkb-potassium-event","event_type":"biochemical_relationship","label":"Potassium deficiency can be downstream of defective chloride transport.","description":"Affected CLCNKB families had hypokalemia alongside salt wasting.","status":"provisional","compartment":null,"participants":[{"entity":{"id":"3f12ade5-3548-5748-a8d4-96ced78dd950","slug":"clcnkb","display_name":"Chloride channel ClC-Kb","entity_type_key":"protein"},"role":"subject","stoichiometry":null,"state_label":"","sequence_order":0,"notes":""},{"entity":{"id":"bb23d568-e85f-5bdd-b264-92d73b8dce53","slug":"plasma-potassium-concentration","display_name":"Plasma potassium concentration","entity_type_key":"cellular_process"},"role":"target","stoichiometry":null,"state_label":"","sequence_order":1,"notes":""}]},"contexts":[{"dimension":"availability_state","value_text":"machinery_impairment","comparator":null,"unit":null,"notes":"Imported condition classification; unverified.","entity":null},{"dimension":"evidence_span","value_text":"{\"source_cache\": \"artifacts/chloride-research/9326936.abstract.txt\", \"locator\": \"Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets\", \"file_sha256\": \"80ade45b4ae654e5aa13b671daebab418640aa033aca3a74cae4ccf52d4e279e\", \"start_char\": 0, \"end_char\": 1227, \"text_sha256\": \"80ade45b4ae654e5aa13b671daebab418640aa033aca3a74cae4ccf52d4e279e\"}","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_model","value_text":"Genetics in seventeen kindreds","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"exposure","value_text":"Loss-of-function CLCNKB variants","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"This cohort had normal magnesium and variable calciuria; do not universalize the full phenotype.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"nutrient_topic","value_text":"Chloride research collection; topical membership is not evidence of a direct dietary effect.","comparator":null,"unit":null,"notes":"","entity":{"slug":"chloride","display_name":"Chloride","entity_type_key":"nutrient_element"}},{"dimension":"organism","value_text":"Human","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"plain_language","value_text":"Potassium deficiency can be downstream of defective chloride transport.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"[chloride-p9326936] Mutations in the chloride channel gene, CLCNKB, cause Bartter's syndrome type III. (1997). https://pubmed.ncbi.nlm.nih.gov/9326936/ DOI: 10.1038/ng1097-171","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"Renal salt handling","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":"93b22145-4c8a-5e5a-8511-69a8a07a1dbe","evidence_kind":"source_excerpt","locator":"Lines 900-911","start_line":900,"end_line":911,"excerpt":"### chloride-clcnkb-potassium\nAffected CLCNKB families had hypokalemia alongside salt wasting.\nCondition category: machinery_impairment\nnutrient_topic: Chloride research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: Potassium deficiency can be downstream of defective chloride transport.\norganism: Human\ntissue_or_cell_type: Renal salt handling\nexperimental_model: Genetics in seventeen kindreds\nlimitations: This cohort had normal magnesium and variable calciuria; do not universalize the full phenotype.\nexposure: Loss-of-function CLCNKB variants\nevidence_span: {\"source_cache\": \"artifacts/chloride-research/9326936.abstract.txt\", \"locator\": \"Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets\", \"file_sha256\": \"80ade45b4ae654e5aa13b671daebab418640aa033aca3a74cae4ccf52d4e279e\", \"start_char\": 0, \"end_char\": 1227, \"text_sha256\": \"80ade45b4ae654e5aa13b671daebab418640aa033aca3a74cae4ccf52d4e279e\"}\n[chloride-p9326936] Mutations in the chloride channel gene, CLCNKB, cause Bartter's syndrome type III. 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