Component

TRPV5

Independent biological entity. Read linked claims for experimental scope and context.

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 it acts on

  1. Cloned rabbit ECaC, now termed TRPV5, confers calcium influx when expressed in Xenopus oocytes.

    TRPV5 → Calcium ion source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Rabbit ECaC/TRPV5 cloning, epithelial localization and expression in Xenopus oocytes
    limitations
    Expression assay; epithelial localization supports an apical role but does not quantify all renal calcium transport.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Oryctolagus cuniculus channel in Xenopus laevis
    plain_language
    TRPV5 provides a calcium entry channel.
    primary_references
    [hoenderop1999] Molecular identification of the apical Ca2+ channel in 1,25-dihydroxyvitamin D3-responsive epithelia (1999). https://pubmed.ncbi.nlm.nih.gov/10085067/ DOI: 10.1074/jbc.274.13.8375
    tissue_or_cell_type
    Plasma membrane; renal epithelial channel origin
    transport_effect
    raises Confers calcium influx when expressed.
    transport_or_reaction_direction
    inward
    transport_pool
    cytosolic calcium Confers calcium influx when expressed.

    Calcium: mechanism-first literature curation (2026-09-17) · lines 375–385

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rabbit ECaC/TRPV5 cloning, epithelial localization and expression in Xenopus oocytes · source_derived_draft · unverified_draft

    ### trpv5-direct-calcium-permeation Cloned rabbit ECaC, now termed TRPV5, confers calcium influx when expressed in Xenopus oocytes. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: TRPV5 provides a calcium entry channel. organism: Oryctolagus cuniculus channel in Xenopus laevis tissue_or_cell_type: Plasma membrane; renal epithelial channel origin experimental_model: Rabbit ECaC/TRPV5 cloning, epithelial localization and expression in Xenopus oocytes limitations: Expression assay; epithelial localization supports an apical role but does not quantify all renal calcium transport. transport_or_reaction_direction: inward [hoenderop1999] Molecular identification of the apical Ca2+ channel in 1,25-dihydroxyvitamin D3-responsive epithelia (1999). https://pubmed.ncbi.nlm.nih.gov/10085067/ DOI: 10.1074/jbc.274.13.8375
    Complete structured claim and evidence

  2. Trpv5-null mice show increased intestinal absorption of orally administered calcium tracer.

    TRPV5 → Intestinal calcium absorption source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    experimental_model
    Trpv5 knockout mice; renal micropuncture and oral calcium tracer assays
    limitations
    Compensation accompanies renal loss; not direct intestinal TRPV5 transport.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Mus musculus
    plain_language
    Gut uptake compensates for kidney losses.
    primary_references
    [hoenderop2003] Renal Ca2+ wasting, hyperabsorption, and reduced bone thickness in mice lacking TRPV5 (2003). https://pmc.ncbi.nlm.nih.gov/articles/PMC297001/ DOI: 10.1172/JCI19826
    tissue_or_cell_type
    Intestine
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Calcium: mechanism-first literature curation (2026-09-17) · lines 247–256

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Trpv5 knockout mice; renal micropuncture and oral calcium tracer assays · source_derived_draft · unverified_draft

    ### trpv5-loss-compensatory-intestinal-absorption Trpv5-null mice show increased intestinal absorption of orally administered calcium tracer. Condition category: machinery_impairment nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Gut uptake compensates for kidney losses. organism: Mus musculus tissue_or_cell_type: Intestine experimental_model: Trpv5 knockout mice; renal micropuncture and oral calcium tracer assays limitations: Compensation accompanies renal loss; not direct intestinal TRPV5 transport. [hoenderop2003] Renal Ca2+ wasting, hyperabsorption, and reduced bone thickness in mice lacking TRPV5 (2003). https://pmc.ncbi.nlm.nih.gov/articles/PMC297001/ DOI: 10.1172/JCI19826
    Complete structured claim and evidence

  3. Trpv5-null mice have impaired distal calcium reabsorption and severe hypercalciuria despite increased vitamin D levels.

    TRPV5 → Renal calcium reabsorption source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    experimental_model
    Trpv5 knockout mice; renal micropuncture and oral calcium tracer assays
    limitations
    Mouse knockout with micropuncture localization.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Mus musculus
    plain_language
    Hormonal compensation cannot replace the missing channel.
    primary_references
    [hoenderop2003] Renal Ca2+ wasting, hyperabsorption, and reduced bone thickness in mice lacking TRPV5 (2003). https://pmc.ncbi.nlm.nih.gov/articles/PMC297001/ DOI: 10.1172/JCI19826
    tissue_or_cell_type
    Early distal convolution
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Calcium: mechanism-first literature curation (2026-09-17) · lines 236–245

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Trpv5 knockout mice; renal micropuncture and oral calcium tracer assays · source_derived_draft · unverified_draft

    ### trpv5-loss-renal-reabsorption Trpv5-null mice have impaired distal calcium reabsorption and severe hypercalciuria despite increased vitamin D levels. Condition category: machinery_impairment nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Hormonal compensation cannot replace the missing channel. organism: Mus musculus tissue_or_cell_type: Early distal convolution experimental_model: Trpv5 knockout mice; renal micropuncture and oral calcium tracer assays limitations: Mouse knockout with micropuncture localization. [hoenderop2003] Renal Ca2+ wasting, hyperabsorption, and reduced bone thickness in mice lacking TRPV5 (2003). https://pmc.ncbi.nlm.nih.gov/articles/PMC297001/ DOI: 10.1172/JCI19826
    Complete structured claim and evidence

What acts on it

  1. FGF23 increases renal distal-tubular TRPV5 membrane abundance through FGFR/alpha-Klotho signaling involving ERK1/2, SGK1 and WNK4.

    Fibroblast growth factor 23 / FGF23 → TRPV5 source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Mouse Fgf23/Klotho/Vdr genetic models, recombinant FGF23, isolated tubules and kidney slices
    limitations
    Mouse genetic/pharmacological models; no claim of equivalent human effect magnitude.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Mus musculus
    plain_language
    FGF23 can help kidneys retain calcium.
    primary_references
    [andrukhova2014] FGF23 promotes renal calcium reabsorption through the TRPV5 channel (2014). https://pmc.ncbi.nlm.nih.gov/articles/PMC3983685/ DOI: 10.1002/embj.201284188
    tissue_or_cell_type
    Renal distal tubules

    Calcium: mechanism-first literature curation (2026-09-17) · lines 124–133

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse Fgf23/Klotho/Vdr genetic models, recombinant FGF23, isolated tubules and kidney slices · source_derived_draft · unverified_draft

    ### fgf23-increases-trpv5-membrane-abundance FGF23 increases renal distal-tubular TRPV5 membrane abundance through FGFR/alpha-Klotho signaling involving ERK1/2, SGK1 and WNK4. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: FGF23 can help kidneys retain calcium. organism: Mus musculus tissue_or_cell_type: Renal distal tubules experimental_model: Mouse Fgf23/Klotho/Vdr genetic models, recombinant FGF23, isolated tubules and kidney slices limitations: Mouse genetic/pharmacological models; no claim of equivalent human effect magnitude. [andrukhova2014] FGF23 promotes renal calcium reabsorption through the TRPV5 channel (2014). https://pmc.ncbi.nlm.nih.gov/articles/PMC3983685/ DOI: 10.1002/embj.201284188
    Complete structured claim and evidence

  2. PTH increases TRPV5 activity through cAMP-PKA-dependent phosphorylation at T709 in receptor/channel expression assays.

    Parathyroid hormone / PTH → TRPV5 source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    HEK293 expression, calcium uptake, FRET, patch clamp and TRPV5 mutagenesis
    limitations
    Response required strong intracellular calcium buffering; cultured-cell mechanism.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Heterologous HEK293 expression system
    plain_language
    PTH can increase calcium entry through TRPV5.
    primary_references
    [degroot2009] Parathyroid hormone activates TRPV5 via PKA-dependent phosphorylation (2009). https://pmc.ncbi.nlm.nih.gov/articles/PMC2723979/ DOI: 10.1681/ASN.2008080873
    tissue_or_cell_type
    Plasma membrane; distal-nephron mechanism

    Calcium: mechanism-first literature curation (2026-09-17) · lines 58–67

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · HEK293 expression, calcium uptake, FRET, patch clamp and TRPV5 mutagenesis · source_derived_draft · unverified_draft

    ### pth-activates-trpv5 PTH increases TRPV5 activity through cAMP-PKA-dependent phosphorylation at T709 in receptor/channel expression assays. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: PTH can increase calcium entry through TRPV5. organism: Heterologous HEK293 expression system tissue_or_cell_type: Plasma membrane; distal-nephron mechanism experimental_model: HEK293 expression, calcium uptake, FRET, patch clamp and TRPV5 mutagenesis limitations: Response required strong intracellular calcium buffering; cultured-cell mechanism. [degroot2009] Parathyroid hormone activates TRPV5 via PKA-dependent phosphorylation (2009). https://pmc.ncbi.nlm.nih.gov/articles/PMC2723979/ DOI: 10.1681/ASN.2008080873
    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