Component
Chloride channel ClC-Kb
Canonical protein; experimental species, state, expression context and nutritional dependence are specified per claim.
3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What it acts on
Affected CLCNKB families had hypokalemia alongside salt wasting.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_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"}
- experimental_model
- Genetics in seventeen kindreds
- exposure
- Loss-of-function CLCNKB variants
- limitations
- This cohort had normal magnesium and variable calciuria; do not universalize the full phenotype.
- nutrient_topic
- Chloride research collection; topical membership is not evidence of a direct dietary effect. · Chloride
- organism
- Human
- plain_language
- Potassium deficiency can be downstream of defective chloride transport.
- primary_references
- [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
- tissue_or_cell_type
- Renal salt handling
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Chloride: transport, acid-base balance, nutrient interactions and loss states (2026-09-17) · lines 900–911
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Genetics in seventeen kindreds · source_derived_draft · unverified_draft
### chloride-clcnkb-potassium Affected CLCNKB families had hypokalemia alongside salt wasting. Condition category: machinery_impairment nutrient_topic: Chloride research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium deficiency can be downstream of defective chloride transport. organism: Human tissue_or_cell_type: Renal salt handling experimental_model: Genetics in seventeen kindreds limitations: This cohort had normal magnesium and variable calciuria; do not universalize the full phenotype. exposure: Loss-of-function CLCNKB variants evidence_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"} [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
Complete structured claim and evidenceCLCNKB loss-of-function variants caused renal salt-wasting hypokalemic alkalosis in the studied families.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_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"}
- experimental_model
- Genetics in seventeen kindreds
- exposure
- Loss-of-function CLCNKB variants
- limitations
- This cohort had normal magnesium and variable calciuria; do not universalize the full phenotype.
- nutrient_topic
- Chloride research collection; topical membership is not evidence of a direct dietary effect. · Chloride
- organism
- Human
- plain_language
- A chloride-channel defect can drive loss of other electrolytes.
- primary_references
- [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
- tissue_or_cell_type
- Renal salt handling
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Chloride: transport, acid-base balance, nutrient interactions and loss states (2026-09-17) · lines 887–898
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Genetics in seventeen kindreds · source_derived_draft · unverified_draft
### chloride-clcnkb-salt CLCNKB loss-of-function variants caused renal salt-wasting hypokalemic alkalosis in the studied families. Condition category: machinery_impairment nutrient_topic: Chloride research collection; topical membership is not evidence of a direct dietary effect. plain_language: A chloride-channel defect can drive loss of other electrolytes. organism: Human tissue_or_cell_type: Renal salt handling experimental_model: Genetics in seventeen kindreds limitations: This cohort had normal magnesium and variable calciuria; do not universalize the full phenotype. exposure: Loss-of-function CLCNKB variants evidence_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"} [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
Complete structured claim and evidence
Where it participates (unsigned role)
Low-K medium lowered intracellular chloride in HEK293 and mDCT cells; depolarizing Kir4.1 mutants increased it.
Experimental context and source evidence
- cross_nutrient
- Extracellular K controls the intracellular chloride signal.
- evidence_location
- Figure 6A-B; Figure S5.
- experimental_model
- Cell culture and Kir4.1 mutant comparisons
- limitations
- HEK chloride and WNK expression differ from native DCT.
- nutrient_topic
- Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
- organism
- Homo sapiens; Mus musculus cell lines
- plain_language
- A change outside the cell can change chloride inside, connecting potassium sensing to salt transport.
- primary_references
- [terker-2015-k-voltage-chloride] Potassium Modulates Electrolyte Balance and Blood Pressure through Effects on Distal Cell Voltage and Chloride (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4332769/ DOI: 10.1016/j.cmet.2014.12.006
- tissue_or_cell_type
- HEK293 and mDCT cells
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 125–136
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell culture and Kir4.1 mutant comparisons · source_derived_draft · unverified_draft
### renal-low-external-k-lowers-cell-chloride Low-K medium lowered intracellular chloride in HEK293 and mDCT cells; depolarizing Kir4.1 mutants increased it. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A change outside the cell can change chloride inside, connecting potassium sensing to salt transport. organism: Homo sapiens; Mus musculus cell lines tissue_or_cell_type: HEK293 and mDCT cells experimental_model: Cell culture and Kir4.1 mutant comparisons limitations: HEK chloride and WNK expression differ from native DCT. cross_nutrient: Extracellular K controls the intracellular chloride signal. evidence_location: Figure 6A-B; Figure S5. [terker-2015-k-voltage-chloride] Potassium Modulates Electrolyte Balance and Blood Pressure through Effects on Distal Cell Voltage and Chloride (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4332769/ DOI: 10.1016/j.cmet.2014.12.006
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.