Component

Mouse pendrin / Slc26a4

Mouse pendrin / Slc26a4. Species, exposure and limitations are retained in each linked claim.

4 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.

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. Pendrin-null collecting ducts had reduced apical chloride/bicarbonate exchange and impaired bicarbonate secretion.

    Mouse pendrin / Slc26a4 → Renal bicarbonate secretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/chloride-research/20375274.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8ddda637993b80b24351aefe0451312d849175bd3ec2f3af23b72b50f7439953", "start_char": 0, "end_char": 1797, "text_sha256": "8ddda637993b80b24351aefe0451312d849175bd3ec2f3af23b72b50f7439953"}
    experimental_model
    Pendrin knockout and isolated collecting-duct perfusion
    exposure
    Slc26a4 deletion
    limitations
    Residual exchange remained; baseline urine chloride excretion was unchanged.
    nutrient_topic
    Chloride research collection; topical membership is not evidence of a direct dietary effect. · Chloride
    organism
    Mouse
    plain_language
    The kidney uses chloride exchange to help dispose of bicarbonate.
    primary_references
    [chloride-p20375274] Deletion of the anion exchanger Slc26a4 (pendrin) decreases apical Cl(-)/HCO3(-) exchanger activity and impairs bicarbonate secretion in kidney collecting duct. (2010). https://pubmed.ncbi.nlm.nih.gov/20375274/ DOI: 10.1152/ajpcell.00033.2010
    tissue_or_cell_type
    Non-acid-secreting intercalated cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Chloride: transport, acid-base balance, nutrient interactions and loss states (2026-09-17) · lines 510–521

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Pendrin knockout and isolated collecting-duct perfusion · source_derived_draft · unverified_draft

    ### chloride-pendrin-bicarbonate Pendrin-null collecting ducts had reduced apical chloride/bicarbonate exchange and impaired bicarbonate secretion. Condition category: machinery_impairment nutrient_topic: Chloride research collection; topical membership is not evidence of a direct dietary effect. plain_language: The kidney uses chloride exchange to help dispose of bicarbonate. organism: Mouse tissue_or_cell_type: Non-acid-secreting intercalated cells experimental_model: Pendrin knockout and isolated collecting-duct perfusion limitations: Residual exchange remained; baseline urine chloride excretion was unchanged. exposure: Slc26a4 deletion evidence_span: {"source_cache": "artifacts/chloride-research/20375274.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8ddda637993b80b24351aefe0451312d849175bd3ec2f3af23b72b50f7439953", "start_char": 0, "end_char": 1797, "text_sha256": "8ddda637993b80b24351aefe0451312d849175bd3ec2f3af23b72b50f7439953"} [chloride-p20375274] Deletion of the anion exchanger Slc26a4 (pendrin) decreases apical Cl(-)/HCO3(-) exchanger activity and impairs bicarbonate secretion in kidney collecting duct. (2010). https://pubmed.ncbi.nlm.nih.gov/20375274/ DOI: 10.1152/ajpcell.00033.2010
    Complete structured claim and evidence
  2. Serum bicarbonate was 27.4 versus 24 meq/L in pendrin-null and control mice.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/chloride-research/20375274.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8ddda637993b80b24351aefe0451312d849175bd3ec2f3af23b72b50f7439953", "start_char": 0, "end_char": 1797, "text_sha256": "8ddda637993b80b24351aefe0451312d849175bd3ec2f3af23b72b50f7439953"}
    experimental_model
    Pendrin knockout and isolated collecting-duct perfusion
    exposure
    Slc26a4 deletion
    limitations
    Residual exchange remained; baseline urine chloride excretion was unchanged.
    nutrient_topic
    Chloride research collection; topical membership is not evidence of a direct dietary effect. · Chloride
    organism
    Mouse
    plain_language
    A local transporter defect changed the blood acid–base measurement.
    primary_references
    [chloride-p20375274] Deletion of the anion exchanger Slc26a4 (pendrin) decreases apical Cl(-)/HCO3(-) exchanger activity and impairs bicarbonate secretion in kidney collecting duct. (2010). https://pubmed.ncbi.nlm.nih.gov/20375274/ DOI: 10.1152/ajpcell.00033.2010
    tissue_or_cell_type
    Non-acid-secreting intercalated cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Chloride: transport, acid-base balance, nutrient interactions and loss states (2026-09-17) · lines 523–534

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Pendrin knockout and isolated collecting-duct perfusion · source_derived_draft · unverified_draft

    ### chloride-pendrin-blood-bicarbonate Serum bicarbonate was 27.4 versus 24 meq/L in pendrin-null and control mice. Condition category: machinery_impairment nutrient_topic: Chloride research collection; topical membership is not evidence of a direct dietary effect. plain_language: A local transporter defect changed the blood acid–base measurement. organism: Mouse tissue_or_cell_type: Non-acid-secreting intercalated cells experimental_model: Pendrin knockout and isolated collecting-duct perfusion limitations: Residual exchange remained; baseline urine chloride excretion was unchanged. exposure: Slc26a4 deletion evidence_span: {"source_cache": "artifacts/chloride-research/20375274.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8ddda637993b80b24351aefe0451312d849175bd3ec2f3af23b72b50f7439953", "start_char": 0, "end_char": 1797, "text_sha256": "8ddda637993b80b24351aefe0451312d849175bd3ec2f3af23b72b50f7439953"} [chloride-p20375274] Deletion of the anion exchanger Slc26a4 (pendrin) decreases apical Cl(-)/HCO3(-) exchanger activity and impairs bicarbonate secretion in kidney collecting duct. (2010). https://pubmed.ncbi.nlm.nih.gov/20375274/ DOI: 10.1152/ajpcell.00033.2010
    Complete structured claim and evidence
  3. Isolated-duct results supported parallel pendrin and NDCBE action in electroneutral NaCl absorption.

    Mouse pendrin / Slc26a4 → Renal chloride reabsorption source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/chloride-research/20389022.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e38f38d6be0ba6db309bcc35de163f9dd6db62963c41864ca0b7fe6c24a31ddb", "start_char": 0, "end_char": 1550, "text_sha256": "e38f38d6be0ba6db309bcc35de163f9dd6db62963c41864ca0b7fe6c24a31ddb"}
    experimental_model
    Gene deletion and perfused collecting ducts
    exposure
    Slc4a8, NCC and ENaC perturbations
    limitations
    Mouse electroneutral transport; thiazide sensitivity alone does not identify NCC.
    nutrient_topic
    Chloride research collection; topical membership is not evidence of a direct dietary effect. · Chloride
    organism
    Mouse
    plain_language
    Two separately modeled exchangers cooperate in the proposed route.
    primary_references
    [chloride-p20389022] The Na+-dependent chloride-bicarbonate exchanger SLC4A8 mediates an electroneutral Na+ reabsorption process in the renal cortical collecting ducts of mice. (2010). https://pubmed.ncbi.nlm.nih.gov/20389022/ DOI: 10.1172/jci40145
    tissue_or_cell_type
    Cortical collecting duct

    Chloride: transport, acid-base balance, nutrient interactions and loss states (2026-09-17) · lines 549–560

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Gene deletion and perfused collecting ducts · source_derived_draft · unverified_draft

    ### chloride-pendrin-ndcbe Isolated-duct results supported parallel pendrin and NDCBE action in electroneutral NaCl absorption. Condition category: normal nutrient_topic: Chloride research collection; topical membership is not evidence of a direct dietary effect. plain_language: Two separately modeled exchangers cooperate in the proposed route. organism: Mouse tissue_or_cell_type: Cortical collecting duct experimental_model: Gene deletion and perfused collecting ducts limitations: Mouse electroneutral transport; thiazide sensitivity alone does not identify NCC. exposure: Slc4a8, NCC and ENaC perturbations evidence_span: {"source_cache": "artifacts/chloride-research/20389022.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e38f38d6be0ba6db309bcc35de163f9dd6db62963c41864ca0b7fe6c24a31ddb", "start_char": 0, "end_char": 1550, "text_sha256": "e38f38d6be0ba6db309bcc35de163f9dd6db62963c41864ca0b7fe6c24a31ddb"} [chloride-p20389022] The Na+-dependent chloride-bicarbonate exchanger SLC4A8 mediates an electroneutral Na+ reabsorption process in the renal cortical collecting ducts of mice. (2010). https://pubmed.ncbi.nlm.nih.gov/20389022/ DOI: 10.1172/jci40145
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Slc4a8 deletion abolished the thiazide-sensitive NaCl absorption measured in cortical collecting ducts.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/chloride-research/20389022.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e38f38d6be0ba6db309bcc35de163f9dd6db62963c41864ca0b7fe6c24a31ddb", "start_char": 0, "end_char": 1550, "text_sha256": "e38f38d6be0ba6db309bcc35de163f9dd6db62963c41864ca0b7fe6c24a31ddb"}
    experimental_model
    Gene deletion and perfused collecting ducts
    exposure
    Slc4a8, NCC and ENaC perturbations
    limitations
    Mouse electroneutral transport; thiazide sensitivity alone does not identify NCC.
    nutrient_topic
    Chloride research collection; topical membership is not evidence of a direct dietary effect. · Chloride
    organism
    Mouse
    plain_language
    Sodium and chloride can be reabsorbed through a coupled exchanger system beyond NCC.
    primary_references
    [chloride-p20389022] The Na+-dependent chloride-bicarbonate exchanger SLC4A8 mediates an electroneutral Na+ reabsorption process in the renal cortical collecting ducts of mice. (2010). https://pubmed.ncbi.nlm.nih.gov/20389022/ DOI: 10.1172/jci40145
    tissue_or_cell_type
    Cortical collecting duct

    Chloride: transport, acid-base balance, nutrient interactions and loss states (2026-09-17) · lines 536–547

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Gene deletion and perfused collecting ducts · source_derived_draft · unverified_draft

    ### chloride-ndcbe-sodium Slc4a8 deletion abolished the thiazide-sensitive NaCl absorption measured in cortical collecting ducts. Condition category: normal nutrient_topic: Chloride research collection; topical membership is not evidence of a direct dietary effect. plain_language: Sodium and chloride can be reabsorbed through a coupled exchanger system beyond NCC. organism: Mouse tissue_or_cell_type: Cortical collecting duct experimental_model: Gene deletion and perfused collecting ducts limitations: Mouse electroneutral transport; thiazide sensitivity alone does not identify NCC. exposure: Slc4a8, NCC and ENaC perturbations evidence_span: {"source_cache": "artifacts/chloride-research/20389022.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e38f38d6be0ba6db309bcc35de163f9dd6db62963c41864ca0b7fe6c24a31ddb", "start_char": 0, "end_char": 1550, "text_sha256": "e38f38d6be0ba6db309bcc35de163f9dd6db62963c41864ca0b7fe6c24a31ddb"} [chloride-p20389022] The Na+-dependent chloride-bicarbonate exchanger SLC4A8 mediates an electroneutral Na+ reabsorption process in the renal cortical collecting ducts of mice. (2010). https://pubmed.ncbi.nlm.nih.gov/20389022/ DOI: 10.1172/jci40145
    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