Component

Mouse sodium-phosphate cotransporter NaPi-IIa / Slc34a1

Mouse sodium-phosphate cotransporter NaPi-IIa / Slc34a1. Species, exposure and limitations are retained in each linked claim.

5 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 acts on it

  1. NaPi-2 redistributed toward intracellular vesicles at steady state despite slower internalization.

    Mouse ClC-5 chloride/proton exchanger / Clcn5 → Mouse sodium-phosphate cotransporter NaPi-IIa / Slc34a1 source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/chloride-research/11099045.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4929ed9da0f3702bbd28bf679f79c2dfb13b4e81d23e44327b27bebdcf3a7cca", "start_char": 0, "end_char": 1218, "text_sha256": "4929ed9da0f3702bbd28bf679f79c2dfb13b4e81d23e44327b27bebdcf3a7cca"}
    experimental_model
    Clcn5 knockout and uptake measurements
    exposure
    Clcn5 disruption
    limitations
    The PTH/vitamin-D/hypercalciuria explanation includes proposed downstream steps; do not treat every link as demonstrated.
    nutrient_topic
    Chloride research collection; topical membership is not evidence of a direct dietary effect. · Chloride
    organism
    Mouse
    plain_language
    An endosomal defect changed where the phosphate transporter was located.
    primary_references
    [chloride-p11099045] ClC-5 Cl- -channel disruption impairs endocytosis in a mouse model for Dent's disease. (2000). https://pubmed.ncbi.nlm.nih.gov/11099045/ DOI: 10.1038/35042597
    tissue_or_cell_type
    Proximal renal tubule
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Chloride: transport, acid-base balance, nutrient interactions and loss states (2026-09-17) · lines 718–729

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Clcn5 knockout and uptake measurements · source_derived_draft · unverified_draft

    ### chloride-clc5-napi NaPi-2 redistributed toward intracellular vesicles at steady state despite slower internalization. Condition category: machinery_impairment nutrient_topic: Chloride research collection; topical membership is not evidence of a direct dietary effect. plain_language: An endosomal defect changed where the phosphate transporter was located. organism: Mouse tissue_or_cell_type: Proximal renal tubule experimental_model: Clcn5 knockout and uptake measurements limitations: The PTH/vitamin-D/hypercalciuria explanation includes proposed downstream steps; do not treat every link as demonstrated. exposure: Clcn5 disruption evidence_span: {"source_cache": "artifacts/chloride-research/11099045.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4929ed9da0f3702bbd28bf679f79c2dfb13b4e81d23e44327b27bebdcf3a7cca", "start_char": 0, "end_char": 1218, "text_sha256": "4929ed9da0f3702bbd28bf679f79c2dfb13b4e81d23e44327b27bebdcf3a7cca"} [chloride-p11099045] ClC-5 Cl- -channel disruption impairs endocytosis in a mouse model for Dent's disease. (2000). https://pubmed.ncbi.nlm.nih.gov/11099045/ DOI: 10.1038/35042597
    Complete structured claim and evidence

  2. Renal NaPi-IIa protein expression increased in Slc34a2-null mice.

    Inducible mouse Slc34a2 knockout in the 2009 absorption study → Mouse sodium-phosphate cotransporter NaPi-IIa / Slc34a1 source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/phosphorus-research/19729436.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "db886399fafd3fc4da4c341765ec69ebb7948f4993e271ca6ee6855d8ba7616d", "start_char": 0, "end_char": 1402, "text_sha256": "db886399fafd3fc4da4c341765ec69ebb7948f4993e271ca6ee6855d8ba7616d"}
    experimental_model
    Inducible Slc34a2 knockout, balance measurements and isolated ileum transport
    exposure
    Knockout versus wild type; low-P diet followed by an acute phosphate bolus
    limitations
    Fraction of active transport is not the fraction of total absorption in every diet or species. Normal serum phosphate can coexist with impaired intestinal entry because the kidney compensates.
    nutrient_topic
    Phosphorus research collection; topical membership is not evidence of a direct dietary effect. · Phosphorus
    organism
    Mouse
    plain_language
    The renal transporter increased while intestinal transport was absent.
    primary_references
    [phosphorus-p19729436] Intestinal npt2b plays a major role in phosphate absorption and homeostasis. (2009). https://pubmed.ncbi.nlm.nih.gov/19729436/ DOI: 10.1681/asn.2009050559
    tissue_or_cell_type
    Intestine and compensatory renal handling
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Phosphorus: metabolism, signaling and nutrient connections (2026-09-17) · lines 295–306

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Inducible Slc34a2 knockout, balance measurements and isolated ileum transport · source_derived_draft · unverified_draft

    ### phosphorus-npt2b-npt2a Renal NaPi-IIa protein expression increased in Slc34a2-null mice. Condition category: machinery_impairment nutrient_topic: Phosphorus research collection; topical membership is not evidence of a direct dietary effect. plain_language: The renal transporter increased while intestinal transport was absent. organism: Mouse tissue_or_cell_type: Intestine and compensatory renal handling experimental_model: Inducible Slc34a2 knockout, balance measurements and isolated ileum transport limitations: Fraction of active transport is not the fraction of total absorption in every diet or species. Normal serum phosphate can coexist with impaired intestinal entry because the kidney compensates. exposure: Knockout versus wild type; low-P diet followed by an acute phosphate bolus evidence_span: {"source_cache": "artifacts/phosphorus-research/19729436.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "db886399fafd3fc4da4c341765ec69ebb7948f4993e271ca6ee6855d8ba7616d", "start_char": 0, "end_char": 1402, "text_sha256": "db886399fafd3fc4da4c341765ec69ebb7948f4993e271ca6ee6855d8ba7616d"} [phosphorus-p19729436] Intestinal npt2b plays a major role in phosphate absorption and homeostasis. (2009). https://pubmed.ncbi.nlm.nih.gov/19729436/ DOI: 10.1681/asn.2009050559
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. NaPi-IIa-knockout mice had approximately 50% lower plasma phosphate and muscle ATP synthetic flux than controls.

    Experimental mouse Slc34a1 / NaPi-IIa knockout → Mouse skeletal-muscle ATP synthetic flux by 31P-MRS source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/phosphorus-research/27338702.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "634bc9a26ebb8d6a911692bcb98a05432db2bc08455c0a02f1ef5e4b953150fe", "start_char": 0, "end_char": 1786, "text_sha256": "634bc9a26ebb8d6a911692bcb98a05432db2bc08455c0a02f1ef5e4b953150fe"}
    experimental_model
    31P-MRS ATP-flux measurements, repletion and cellular/mitochondrial experiments
    exposure
    Diet-induced low phosphate, NaPi-IIa knockout, phosphate repletion; one SLC34A3-associated human case
    limitations
    ATP synthetic flux is not ATP pool size or direct proof that all measured flux is mitochondrial oxidative phosphorylation. One human case cannot define a population threshold.
    nutrient_topic
    Phosphorus research collection; topical membership is not evidence of a direct dietary effect. · Phosphorus
    organism
    Mouse
    plain_language
    A kidney transport defect affected a measurement in muscle.
    primary_references
    [phosphorus-p27338702] Hypophosphatemia promotes lower rates of muscle ATP synthesis. (2016). https://pubmed.ncbi.nlm.nih.gov/27338702/ DOI: 10.1096/fj.201600473r
    tissue_or_cell_type
    Skeletal muscle
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Phosphorus: metabolism, signaling and nutrient connections (2026-09-17) · lines 581–592

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · 31P-MRS ATP-flux measurements, repletion and cellular/mitochondrial experiments · source_derived_draft · unverified_draft

    ### phosphorus-napi2a-atp NaPi-IIa-knockout mice had approximately 50% lower plasma phosphate and muscle ATP synthetic flux than controls. Condition category: machinery_impairment nutrient_topic: Phosphorus research collection; topical membership is not evidence of a direct dietary effect. plain_language: A kidney transport defect affected a measurement in muscle. organism: Mouse tissue_or_cell_type: Skeletal muscle experimental_model: 31P-MRS ATP-flux measurements, repletion and cellular/mitochondrial experiments limitations: ATP synthetic flux is not ATP pool size or direct proof that all measured flux is mitochondrial oxidative phosphorylation. One human case cannot define a population threshold. exposure: Diet-induced low phosphate, NaPi-IIa knockout, phosphate repletion; one SLC34A3-associated human case evidence_span: {"source_cache": "artifacts/phosphorus-research/27338702.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "634bc9a26ebb8d6a911692bcb98a05432db2bc08455c0a02f1ef5e4b953150fe", "start_char": 0, "end_char": 1786, "text_sha256": "634bc9a26ebb8d6a911692bcb98a05432db2bc08455c0a02f1ef5e4b953150fe"} [phosphorus-p27338702] Hypophosphatemia promotes lower rates of muscle ATP synthesis. (2016). https://pubmed.ncbi.nlm.nih.gov/27338702/ DOI: 10.1096/fj.201600473r
    Complete structured claim and evidence

  2. PTH-(3–34), used to stimulate apical receptors, failed to induce NaPi-IIa internalization in Nherf1-deficient mice.

    PTH-(3–34) experimental peptide → Mouse renal NaPi-IIa internalization from the brush border source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/phosphorus-research/16987995.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c5a055252ffc61da98e24d1de3a1733ee7aea678aded8cbdf071d18ad707d0bc", "start_char": 0, "end_char": 1699, "text_sha256": "c5a055252ffc61da98e24d1de3a1733ee7aea678aded8cbdf071d18ad707d0bc"}
    experimental_model
    Receptor-fragment stimulation, knockout and signaling-bypass experiments
    exposure
    PTH-(1–34), apically selective PTH-(3–34), PKC/PKA pathway stimulation
    limitations
    Apical and basolateral receptor routes differ. Loss of one scaffold does not eliminate every PTH response.
    nutrient_topic
    Phosphorus research collection; topical membership is not evidence of a direct dietary effect. · Phosphorus
    organism
    Mouse
    plain_language
    The isolated apical route failed, unlike the broader PTH-(1–34) stimulation.
    primary_references
    [phosphorus-p16987995] Defective coupling of apical PTH receptors to phospholipase C prevents internalization of the Na+-phosphate cotransporter NaPi-IIa in Nherf1-deficient mice. (2007). https://pubmed.ncbi.nlm.nih.gov/16987995/ DOI: 10.1152/ajpcell.00126.2006
    tissue_or_cell_type
    Renal proximal tubule brush-border membrane
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Phosphorus: metabolism, signaling and nutrient connections (2026-09-17) · lines 425–436

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Receptor-fragment stimulation, knockout and signaling-bypass experiments · source_derived_draft · unverified_draft

    ### phosphorus-nherf-napi PTH-(3–34), used to stimulate apical receptors, failed to induce NaPi-IIa internalization in Nherf1-deficient mice. Condition category: machinery_impairment nutrient_topic: Phosphorus research collection; topical membership is not evidence of a direct dietary effect. plain_language: The isolated apical route failed, unlike the broader PTH-(1–34) stimulation. organism: Mouse tissue_or_cell_type: Renal proximal tubule brush-border membrane experimental_model: Receptor-fragment stimulation, knockout and signaling-bypass experiments limitations: Apical and basolateral receptor routes differ. Loss of one scaffold does not eliminate every PTH response. exposure: PTH-(1–34), apically selective PTH-(3–34), PKC/PKA pathway stimulation evidence_span: {"source_cache": "artifacts/phosphorus-research/16987995.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c5a055252ffc61da98e24d1de3a1733ee7aea678aded8cbdf071d18ad707d0bc", "start_char": 0, "end_char": 1699, "text_sha256": "c5a055252ffc61da98e24d1de3a1733ee7aea678aded8cbdf071d18ad707d0bc"} [phosphorus-p16987995] Defective coupling of apical PTH receptors to phospholipase C prevents internalization of the Na+-phosphate cotransporter NaPi-IIa in Nherf1-deficient mice. (2007). https://pubmed.ncbi.nlm.nih.gov/16987995/ DOI: 10.1152/ajpcell.00126.2006
    Complete structured claim and evidence

  3. PTH-(1–34) induced NaPi-IIa internalization in both wild-type and Nherf1-deficient mice.

    PTH-(1–34) experimental peptide → Mouse renal NaPi-IIa internalization from the brush border source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/phosphorus-research/16987995.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c5a055252ffc61da98e24d1de3a1733ee7aea678aded8cbdf071d18ad707d0bc", "start_char": 0, "end_char": 1699, "text_sha256": "c5a055252ffc61da98e24d1de3a1733ee7aea678aded8cbdf071d18ad707d0bc"}
    experimental_model
    Receptor-fragment stimulation, knockout and signaling-bypass experiments
    exposure
    PTH-(1–34), apically selective PTH-(3–34), PKC/PKA pathway stimulation
    limitations
    Apical and basolateral receptor routes differ. Loss of one scaffold does not eliminate every PTH response.
    nutrient_topic
    Phosphorus research collection; topical membership is not evidence of a direct dietary effect. · Phosphorus
    organism
    Mouse
    plain_language
    PTH could remove the transporter from the brush border even when one scaffold was absent.
    primary_references
    [phosphorus-p16987995] Defective coupling of apical PTH receptors to phospholipase C prevents internalization of the Na+-phosphate cotransporter NaPi-IIa in Nherf1-deficient mice. (2007). https://pubmed.ncbi.nlm.nih.gov/16987995/ DOI: 10.1152/ajpcell.00126.2006
    tissue_or_cell_type
    Renal proximal tubule brush-border membrane

    Phosphorus: metabolism, signaling and nutrient connections (2026-09-17) · lines 399–410

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Receptor-fragment stimulation, knockout and signaling-bypass experiments · source_derived_draft · unverified_draft

    ### phosphorus-pth-internalization PTH-(1–34) induced NaPi-IIa internalization in both wild-type and Nherf1-deficient mice. Condition category: normal nutrient_topic: Phosphorus research collection; topical membership is not evidence of a direct dietary effect. plain_language: PTH could remove the transporter from the brush border even when one scaffold was absent. organism: Mouse tissue_or_cell_type: Renal proximal tubule brush-border membrane experimental_model: Receptor-fragment stimulation, knockout and signaling-bypass experiments limitations: Apical and basolateral receptor routes differ. Loss of one scaffold does not eliminate every PTH response. exposure: PTH-(1–34), apically selective PTH-(3–34), PKC/PKA pathway stimulation evidence_span: {"source_cache": "artifacts/phosphorus-research/16987995.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c5a055252ffc61da98e24d1de3a1733ee7aea678aded8cbdf071d18ad707d0bc", "start_char": 0, "end_char": 1699, "text_sha256": "c5a055252ffc61da98e24d1de3a1733ee7aea678aded8cbdf071d18ad707d0bc"} [phosphorus-p16987995] Defective coupling of apical PTH receptors to phospholipase C prevents internalization of the Na+-phosphate cotransporter NaPi-IIa in Nherf1-deficient mice. (2007). https://pubmed.ncbi.nlm.nih.gov/16987995/ DOI: 10.1152/ajpcell.00126.2006
    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.

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