Component

Mouse ClC-K2 basolateral chloride channel / Clcnk2

Mouse ClC-K2 basolateral chloride channel / Clcnk2. Species, exposure and limitations are retained in each linked claim.

2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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.

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.

Recorded relationships

What it acts on

  1. Knockout patch-clamp studies identified ClC-K2 as a major basolateral chloride channel in the tested nephron segments.

    Mouse ClC-K2 basolateral chloride channel / Clcnk2 → Renal chloride reabsorption source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/chloride-research/27335120.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a0a14e0cc6fd76c451f92665dfed0255edcaf0355b46414f91c74d977f5d6b3", "start_char": 0, "end_char": 1432, "text_sha256": "0a0a14e0cc6fd76c451f92665dfed0255edcaf0355b46414f91c74d977f5d6b3"}
    experimental_model
    Clcnk2 knockout and nephron patch clamp
    exposure
    Gene deletion; furosemide/thiazide responses
    limitations
    Mouse ortholog; not a claim of dietary chloride deficiency.
    nutrient_topic
    Chloride research collection; topical membership is not evidence of a direct dietary effect. · Chloride
    organism
    Mouse
    plain_language
    Chloride needs a route out of the back of kidney cells as well as a route in.
    primary_references
    [chloride-p27335120] The ClC-K2 Chloride Channel Is Critical for Salt Handling in the Distal Nephron. (2017). https://pubmed.ncbi.nlm.nih.gov/27335120/ DOI: 10.1681/asn.2016010085
    tissue_or_cell_type
    Thick ascending limb and distal nephron

    Chloride: transport, acid-base balance, nutrient interactions and loss states (2026-09-17) · lines 913–924

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Clcnk2 knockout and nephron patch clamp · source_derived_draft · unverified_draft

    ### chloride-clcnk2-basolateral Knockout patch-clamp studies identified ClC-K2 as a major basolateral chloride channel in the tested nephron segments. Condition category: normal nutrient_topic: Chloride research collection; topical membership is not evidence of a direct dietary effect. plain_language: Chloride needs a route out of the back of kidney cells as well as a route in. organism: Mouse tissue_or_cell_type: Thick ascending limb and distal nephron experimental_model: Clcnk2 knockout and nephron patch clamp limitations: Mouse ortholog; not a claim of dietary chloride deficiency. exposure: Gene deletion; furosemide/thiazide responses evidence_span: {"source_cache": "artifacts/chloride-research/27335120.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a0a14e0cc6fd76c451f92665dfed0255edcaf0355b46414f91c74d977f5d6b3", "start_char": 0, "end_char": 1432, "text_sha256": "0a0a14e0cc6fd76c451f92665dfed0255edcaf0355b46414f91c74d977f5d6b3"} [chloride-p27335120] The ClC-K2 Chloride Channel Is Critical for Salt Handling in the Distal Nephron. (2017). https://pubmed.ncbi.nlm.nih.gov/27335120/ DOI: 10.1681/asn.2016010085
    Complete structured claim and evidence

  2. ClC-K2-null mice lacked the usual furosemide natriuretic response and had a severely blunted thiazide response.

    Mouse ClC-K2 basolateral chloride channel / Clcnk2 → Renal response to loop diuretics source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/chloride-research/27335120.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a0a14e0cc6fd76c451f92665dfed0255edcaf0355b46414f91c74d977f5d6b3", "start_char": 0, "end_char": 1432, "text_sha256": "0a0a14e0cc6fd76c451f92665dfed0255edcaf0355b46414f91c74d977f5d6b3"}
    experimental_model
    Clcnk2 knockout and nephron patch clamp
    exposure
    Gene deletion; furosemide/thiazide responses
    limitations
    Mouse ortholog; not a claim of dietary chloride deficiency.
    nutrient_topic
    Chloride research collection; topical membership is not evidence of a direct dietary effect. · Chloride
    organism
    Mouse
    plain_language
    A transporter defect changed how two diuretic classes worked.
    primary_references
    [chloride-p27335120] The ClC-K2 Chloride Channel Is Critical for Salt Handling in the Distal Nephron. (2017). https://pubmed.ncbi.nlm.nih.gov/27335120/ DOI: 10.1681/asn.2016010085
    tissue_or_cell_type
    Thick ascending limb and distal nephron
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Chloride: transport, acid-base balance, nutrient interactions and loss states (2026-09-17) · lines 926–937

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Clcnk2 knockout and nephron patch clamp · source_derived_draft · unverified_draft

    ### chloride-clcnk2-diuretics ClC-K2-null mice lacked the usual furosemide natriuretic response and had a severely blunted thiazide response. Condition category: machinery_impairment nutrient_topic: Chloride research collection; topical membership is not evidence of a direct dietary effect. plain_language: A transporter defect changed how two diuretic classes worked. organism: Mouse tissue_or_cell_type: Thick ascending limb and distal nephron experimental_model: Clcnk2 knockout and nephron patch clamp limitations: Mouse ortholog; not a claim of dietary chloride deficiency. exposure: Gene deletion; furosemide/thiazide responses evidence_span: {"source_cache": "artifacts/chloride-research/27335120.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a0a14e0cc6fd76c451f92665dfed0255edcaf0355b46414f91c74d977f5d6b3", "start_char": 0, "end_char": 1432, "text_sha256": "0a0a14e0cc6fd76c451f92665dfed0255edcaf0355b46414f91c74d977f5d6b3"} [chloride-p27335120] The ClC-K2 Chloride Channel Is Critical for Salt Handling in the Distal Nephron. (2017). https://pubmed.ncbi.nlm.nih.gov/27335120/ DOI: 10.1681/asn.2016010085
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards