Component

Mouse gastric anion transporter Slc26a9

Mouse gastric anion transporter Slc26a9. 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. Slc26a9-null mice lost gastric acid secretion at five weeks.

    Mouse gastric anion transporter Slc26a9 → Gastric acid secretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/chloride-research/19004773.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ed1a2033c883ec9b4eeab6a9c0bae03d1f478adf66913c3d5e8c43879a836d3e", "start_char": 0, "end_char": 1342, "text_sha256": "ed1a2033c883ec9b4eeab6a9c0bae03d1f478adf66913c3d5e8c43879a836d3e"}
    experimental_model
    Slc26a9 deletion and heterologous transport assays
    exposure
    Knockout at five weeks; expression assays
    limitations
    Different assays showed conductance or exchange; do not assign one universal stoichiometry.
    nutrient_topic
    Chloride research collection; topical membership is not evidence of a direct dietary effect. · Chloride
    organism
    Mouse protein; oocytes and cultured cells
    plain_language
    A second chloride-handling protein is needed for normal acid secretion in this model.
    primary_references
    [chloride-p19004773] Deletion of the chloride transporter Slc26a9 causes loss of tubulovesicles in parietal cells and impairs acid secretion in the stomach. (2008). https://pubmed.ncbi.nlm.nih.gov/19004773/ DOI: 10.1073/pnas.0800616105
    tissue_or_cell_type
    Gastric parietal cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Chloride: transport, acid-base balance, nutrient interactions and loss states (2026-09-17) · lines 198–209

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Slc26a9 deletion and heterologous transport assays · source_derived_draft · unverified_draft

    ### chloride-slc26a9-acid Slc26a9-null mice lost gastric acid secretion at five weeks. Condition category: machinery_impairment nutrient_topic: Chloride research collection; topical membership is not evidence of a direct dietary effect. plain_language: A second chloride-handling protein is needed for normal acid secretion in this model. organism: Mouse protein; oocytes and cultured cells tissue_or_cell_type: Gastric parietal cells experimental_model: Slc26a9 deletion and heterologous transport assays limitations: Different assays showed conductance or exchange; do not assign one universal stoichiometry. exposure: Knockout at five weeks; expression assays evidence_span: {"source_cache": "artifacts/chloride-research/19004773.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ed1a2033c883ec9b4eeab6a9c0bae03d1f478adf66913c3d5e8c43879a836d3e", "start_char": 0, "end_char": 1342, "text_sha256": "ed1a2033c883ec9b4eeab6a9c0bae03d1f478adf66913c3d5e8c43879a836d3e"} [chloride-p19004773] Deletion of the chloride transporter Slc26a9 causes loss of tubulovesicles in parietal cells and impairs acid secretion in the stomach. (2008). https://pubmed.ncbi.nlm.nih.gov/19004773/ DOI: 10.1073/pnas.0800616105
    Complete structured claim and evidence

  2. Slc26a9 deletion eliminated parietal-cell tubulovesicles and shifted H-K-ATPase localization to the apical pole.

    Mouse gastric anion transporter Slc26a9 → Gastric parietal-cell secretory membrane organization source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/chloride-research/19004773.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ed1a2033c883ec9b4eeab6a9c0bae03d1f478adf66913c3d5e8c43879a836d3e", "start_char": 0, "end_char": 1342, "text_sha256": "ed1a2033c883ec9b4eeab6a9c0bae03d1f478adf66913c3d5e8c43879a836d3e"}
    experimental_model
    Slc26a9 deletion and heterologous transport assays
    exposure
    Knockout at five weeks; expression assays
    limitations
    Different assays showed conductance or exchange; do not assign one universal stoichiometry.
    nutrient_topic
    Chloride research collection; topical membership is not evidence of a direct dietary effect. · Chloride
    organism
    Mouse protein; oocytes and cultured cells
    plain_language
    The secretory machinery changed as well as the acid output.
    primary_references
    [chloride-p19004773] Deletion of the chloride transporter Slc26a9 causes loss of tubulovesicles in parietal cells and impairs acid secretion in the stomach. (2008). https://pubmed.ncbi.nlm.nih.gov/19004773/ DOI: 10.1073/pnas.0800616105
    tissue_or_cell_type
    Gastric parietal cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Chloride: transport, acid-base balance, nutrient interactions and loss states (2026-09-17) · lines 211–222

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Slc26a9 deletion and heterologous transport assays · source_derived_draft · unverified_draft

    ### chloride-slc26a9-membranes Slc26a9 deletion eliminated parietal-cell tubulovesicles and shifted H-K-ATPase localization to the apical pole. Condition category: machinery_impairment nutrient_topic: Chloride research collection; topical membership is not evidence of a direct dietary effect. plain_language: The secretory machinery changed as well as the acid output. organism: Mouse protein; oocytes and cultured cells tissue_or_cell_type: Gastric parietal cells experimental_model: Slc26a9 deletion and heterologous transport assays limitations: Different assays showed conductance or exchange; do not assign one universal stoichiometry. exposure: Knockout at five weeks; expression assays evidence_span: {"source_cache": "artifacts/chloride-research/19004773.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ed1a2033c883ec9b4eeab6a9c0bae03d1f478adf66913c3d5e8c43879a836d3e", "start_char": 0, "end_char": 1342, "text_sha256": "ed1a2033c883ec9b4eeab6a9c0bae03d1f478adf66913c3d5e8c43879a836d3e"} [chloride-p19004773] Deletion of the chloride transporter Slc26a9 causes loss of tubulovesicles in parietal cells and impairs acid secretion in the stomach. (2008). https://pubmed.ncbi.nlm.nih.gov/19004773/ DOI: 10.1073/pnas.0800616105
    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