Component

Human kidney-specific multidrug and toxin extrusion protein 2 / MATE2-K / SLC47A2

Human kidney-specific multidrug and toxin extrusion protein 2 / MATE2-K / SLC47A2. Species, exposure and limitations are retained in each linked claim.

4 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. hMATE2-K is expressed predominantly in the kidney and localises to the brush-border membranes of proximal tubules, where it transports metformin with a Km of 1.05 mM.

    Human kidney-specific multidrug and toxin extrusion protein 2 / MATE2-K / SLC47A2 → Renal tubular secretion of metformin source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/metformin-research/16807400.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "681a4ea4ae958690a5a707397ee3a2b254ebeaab832292f14beea5716e58a9b2", "start_char": 0, "end_char": 1742, "text_sha256": "681a4ea4ae958690a5a707397ee3a2b254ebeaab832292f14beea5716e58a9b2"}
    experimental_model
    Cloning, expression and kinetic characterisation of hMATE2-K from human kidney
    exposure
    Proton-gradient-dependent antiport; ammonium-chloride-induced intracellular acidification
    limitations
    Kidney-specific expression and substrate list from a transfected system; thiamine appears in the same substrate list, which is an observation about the transporter, not a drug-nutrient competition measurement.
    nutrient_topic
    Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. · Metformin
    organism
    Human transporter
    plain_language
    The exit route sits on the urine-facing side of the kidney tubule.
    primary_references
    [metformin-p16807400] Identification and functional characterization of a new human kidney-specific H+/organic cation antiporter, kidney-specific multidrug and toxin extrusion 2. (2006). https://pubmed.ncbi.nlm.nih.gov/16807400/ DOI: 10.1681/asn.2006030205
    tissue_or_cell_type
    Renal proximal-tubule brush-border membrane

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 242–253

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cloning, expression and kinetic characterisation of hMATE2-K from human kidney · source_derived_draft · unverified_draft

    ### metformin-mate2k-kidney hMATE2-K is expressed predominantly in the kidney and localises to the brush-border membranes of proximal tubules, where it transports metformin with a Km of 1.05 mM. Condition category: normal nutrient_topic: Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. plain_language: The exit route sits on the urine-facing side of the kidney tubule. organism: Human transporter tissue_or_cell_type: Renal proximal-tubule brush-border membrane experimental_model: Cloning, expression and kinetic characterisation of hMATE2-K from human kidney limitations: Kidney-specific expression and substrate list from a transfected system; thiamine appears in the same substrate list, which is an observation about the transporter, not a drug-nutrient competition measurement. exposure: Proton-gradient-dependent antiport; ammonium-chloride-induced intracellular acidification evidence_span: {"source_cache": "artifacts/metformin-research/16807400.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "681a4ea4ae958690a5a707397ee3a2b254ebeaab832292f14beea5716e58a9b2", "start_char": 0, "end_char": 1742, "text_sha256": "681a4ea4ae958690a5a707397ee3a2b254ebeaab832292f14beea5716e58a9b2"} [metformin-p16807400] Identification and functional characterization of a new human kidney-specific H+/organic cation antiporter, kidney-specific multidrug and toxin extrusion 2. (2006). https://pubmed.ncbi.nlm.nih.gov/16807400/ DOI: 10.1681/asn.2006030205
    Complete structured claim and evidence

  2. MATE2-K transported metformin in a proton-gradient-dependent manner, with a Michaelis-Menten constant of 1.98 mM.

    Human kidney-specific multidrug and toxin extrusion protein 2 / MATE2-K / SLC47A2 → Metformin source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/metformin-research/17509534.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d2660dd67050133c958e8aa13cf2ac6b574bd56fcefa116d3a73c3db4a7cea44", "start_char": 0, "end_char": 1841, "text_sha256": "d2660dd67050133c958e8aa13cf2ac6b574bd56fcefa116d3a73c3db4a7cea44"}
    experimental_model
    MATE1 and MATE2-K cDNA transfection into HEK293 cells with kinetic analysis
    exposure
    Oppositely directed proton gradient; Michaelis-Menten constants for ten substrates
    limitations
    Millimolar affinities in a transfected system. Substrate overlap describes a shared route, not a predicted clinical interaction.
    nutrient_topic
    Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. · Metformin
    organism
    Human transporters
    plain_language
    A proton-driven pump moves the drug out of the cell into urine.
    primary_references
    [metformin-p17509534] Substrate specificity of MATE1 and MATE2-K, human multidrug and toxin extrusions/H(+)-organic cation antiporters. (2007). https://pubmed.ncbi.nlm.nih.gov/17509534/ DOI: 10.1016/j.bcp.2007.04.010
    tissue_or_cell_type
    Renal brush-border membrane transport
    transport_effect
    depends Recorded as proton-gradient-dependent transport. MATE carriers run either way with the proton gradient, and the assay's pool and the extrusion role move opposite ways.
    transport_pool
    the renal tubular cell interior Recorded as proton-gradient-dependent transport. MATE carriers run either way with the proton gradient, and the assay's pool and the extrusion role move opposite ways.

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 216–227

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · MATE1 and MATE2-K cDNA transfection into HEK293 cells with kinetic analysis · source_derived_draft · unverified_draft

    ### metformin-mate2k-metformin MATE2-K transported metformin in a proton-gradient-dependent manner, with a Michaelis-Menten constant of 1.98 mM. Condition category: normal nutrient_topic: Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. plain_language: A proton-driven pump moves the drug out of the cell into urine. organism: Human transporters tissue_or_cell_type: Renal brush-border membrane transport experimental_model: MATE1 and MATE2-K cDNA transfection into HEK293 cells with kinetic analysis limitations: Millimolar affinities in a transfected system. Substrate overlap describes a shared route, not a predicted clinical interaction. exposure: Oppositely directed proton gradient; Michaelis-Menten constants for ten substrates evidence_span: {"source_cache": "artifacts/metformin-research/17509534.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d2660dd67050133c958e8aa13cf2ac6b574bd56fcefa116d3a73c3db4a7cea44", "start_char": 0, "end_char": 1841, "text_sha256": "d2660dd67050133c958e8aa13cf2ac6b574bd56fcefa116d3a73c3db4a7cea44"} [metformin-p17509534] Substrate specificity of MATE1 and MATE2-K, human multidrug and toxin extrusions/H(+)-organic cation antiporters. (2007). https://pubmed.ncbi.nlm.nih.gov/17509534/ DOI: 10.1016/j.bcp.2007.04.010
    Complete structured claim and evidence

  3. Intracellular acidification stimulated hMATE2-K-dependent transport of organic cations including metformin and thiamine.

    Human kidney-specific multidrug and toxin extrusion protein 2 / MATE2-K / SLC47A2 → Thiamine (vitamin B1) source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/metformin-research/16807400.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "681a4ea4ae958690a5a707397ee3a2b254ebeaab832292f14beea5716e58a9b2", "start_char": 0, "end_char": 1742, "text_sha256": "681a4ea4ae958690a5a707397ee3a2b254ebeaab832292f14beea5716e58a9b2"}
    experimental_model
    Cloning, expression and kinetic characterisation of hMATE2-K from human kidney
    exposure
    Proton-gradient-dependent antiport; ammonium-chloride-induced intracellular acidification
    limitations
    Kidney-specific expression and substrate list from a transfected system; thiamine appears in the same substrate list, which is an observation about the transporter, not a drug-nutrient competition measurement.
    nutrient_topic
    Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. · Metformin
    organism
    Human transporter
    plain_language
    The same exit pump also handles vitamin B1, so the drug and the vitamin share a route.
    primary_references
    [metformin-p16807400] Identification and functional characterization of a new human kidney-specific H+/organic cation antiporter, kidney-specific multidrug and toxin extrusion 2. (2006). https://pubmed.ncbi.nlm.nih.gov/16807400/ DOI: 10.1681/asn.2006030205
    tissue_or_cell_type
    Renal proximal-tubule brush-border membrane
    transport_effect
    lowers Intracellular acidification stimulated the transport, which is the extrusion direction.
    transport_pool
    the renal tubular cell interior Intracellular acidification stimulated the transport, which is the extrusion direction.

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 255–266

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cloning, expression and kinetic characterisation of hMATE2-K from human kidney · source_derived_draft · unverified_draft

    ### metformin-mate2k-thiamine-substrate Intracellular acidification stimulated hMATE2-K-dependent transport of organic cations including metformin and thiamine. Condition category: normal nutrient_topic: Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. plain_language: The same exit pump also handles vitamin B1, so the drug and the vitamin share a route. organism: Human transporter tissue_or_cell_type: Renal proximal-tubule brush-border membrane experimental_model: Cloning, expression and kinetic characterisation of hMATE2-K from human kidney limitations: Kidney-specific expression and substrate list from a transfected system; thiamine appears in the same substrate list, which is an observation about the transporter, not a drug-nutrient competition measurement. exposure: Proton-gradient-dependent antiport; ammonium-chloride-induced intracellular acidification evidence_span: {"source_cache": "artifacts/metformin-research/16807400.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "681a4ea4ae958690a5a707397ee3a2b254ebeaab832292f14beea5716e58a9b2", "start_char": 0, "end_char": 1742, "text_sha256": "681a4ea4ae958690a5a707397ee3a2b254ebeaab832292f14beea5716e58a9b2"} [metformin-p16807400] Identification and functional characterization of a new human kidney-specific H+/organic cation antiporter, kidney-specific multidrug and toxin extrusion 2. (2006). https://pubmed.ncbi.nlm.nih.gov/16807400/ DOI: 10.1681/asn.2006030205
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. MATE1 and MATE2-K together mediate tubular secretion of intracellular ionic compounds across the kidney brush-border membranes.

    Human multidrug and toxin extrusion protein 1 / MATE1 / SLC47A1 → MATE-mediated metformin efflux across brush-border membranes source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/metformin-research/17509534.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d2660dd67050133c958e8aa13cf2ac6b574bd56fcefa116d3a73c3db4a7cea44", "start_char": 0, "end_char": 1841, "text_sha256": "d2660dd67050133c958e8aa13cf2ac6b574bd56fcefa116d3a73c3db4a7cea44"}
    experimental_model
    MATE1 and MATE2-K cDNA transfection into HEK293 cells with kinetic analysis
    exposure
    Oppositely directed proton gradient; Michaelis-Menten constants for ten substrates
    limitations
    Millimolar affinities in a transfected system. Substrate overlap describes a shared route, not a predicted clinical interaction.
    nutrient_topic
    Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. · Metformin
    organism
    Human transporters
    plain_language
    Entry and exit are separate steps handled by different proteins.
    primary_references
    [metformin-p17509534] Substrate specificity of MATE1 and MATE2-K, human multidrug and toxin extrusions/H(+)-organic cation antiporters. (2007). https://pubmed.ncbi.nlm.nih.gov/17509534/ DOI: 10.1016/j.bcp.2007.04.010
    tissue_or_cell_type
    Renal brush-border membrane transport

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 229–240

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · MATE1 and MATE2-K cDNA transfection into HEK293 cells with kinetic analysis · source_derived_draft · unverified_draft

    ### metformin-mate-detoxication MATE1 and MATE2-K together mediate tubular secretion of intracellular ionic compounds across the kidney brush-border membranes. Condition category: normal nutrient_topic: Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. plain_language: Entry and exit are separate steps handled by different proteins. organism: Human transporters tissue_or_cell_type: Renal brush-border membrane transport experimental_model: MATE1 and MATE2-K cDNA transfection into HEK293 cells with kinetic analysis limitations: Millimolar affinities in a transfected system. Substrate overlap describes a shared route, not a predicted clinical interaction. exposure: Oppositely directed proton gradient; Michaelis-Menten constants for ten substrates evidence_span: {"source_cache": "artifacts/metformin-research/17509534.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d2660dd67050133c958e8aa13cf2ac6b574bd56fcefa116d3a73c3db4a7cea44", "start_char": 0, "end_char": 1841, "text_sha256": "d2660dd67050133c958e8aa13cf2ac6b574bd56fcefa116d3a73c3db4a7cea44"} [metformin-p17509534] Substrate specificity of MATE1 and MATE2-K, human multidrug and toxin extrusions/H(+)-organic cation antiporters. (2007). https://pubmed.ncbi.nlm.nih.gov/17509534/ DOI: 10.1016/j.bcp.2007.04.010
    Complete structured claim and evidence

In the sources

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

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