Component
Alpha-Klotho / KL
Independent biological entity. Read linked claims for experimental scope and context.
3 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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What it acts on
Alpha-Klotho cooperates with FGFR1(IIIc) to confer high-affinity binding and signaling by FGF23.
Experimental context and source evidence
- experimental_model
- Renal homogenates, receptor-reconstitution cell assays and anti-Klotho antibody in mice
- limitations
- Specifically FGFR1(IIIc) reconstitution; not all FGFR1 splice forms are equivalent.
- nutrient_topic
- Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
- organism
- Mammalian cell systems; Mus musculus
- plain_language
- FGF23 needs a suitable receptor partnership.
- primary_references
- [urakawa2006] Klotho converts canonical FGF receptor into a specific receptor for FGF23 (2006). https://pubmed.ncbi.nlm.nih.gov/17086194/ DOI: 10.1038/nature05315
- tissue_or_cell_type
- Kidney receptor system
Calcium: mechanism-first literature curation (2026-09-17) · lines 113–122
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Renal homogenates, receptor-reconstitution cell assays and anti-Klotho antibody in mice · source_derived_draft · unverified_draft
### klotho-fgfr1-fgf23-receptor Alpha-Klotho cooperates with FGFR1(IIIc) to confer high-affinity binding and signaling by FGF23. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: FGF23 needs a suitable receptor partnership. organism: Mammalian cell systems; Mus musculus tissue_or_cell_type: Kidney receptor system experimental_model: Renal homogenates, receptor-reconstitution cell assays and anti-Klotho antibody in mice limitations: Specifically FGFR1(IIIc) reconstitution; not all FGFR1 splice forms are equivalent. [urakawa2006] Klotho converts canonical FGF receptor into a specific receptor for FGF23 (2006). https://pubmed.ncbi.nlm.nih.gov/17086194/ DOI: 10.1038/nature05315
Complete structured claim and evidence
Where it participates (unsigned role)
At 1.0 mM Ca, six-hour exposure to 2.0 versus 0.5 mM Mg increased CaSR mRNA and protein in intact rat glands.
Experimental context and source evidence
- cross_nutrient
- magnesium -> calcium sensing
- experimental_model
- Six-hour ex-vivo gland incubation with receptor expression assays
- limitations
- Receptor abundance alone does not prove altered clinical calcium balance; VDR, FGFR1 and Klotho also rose in this experiment.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Rattus norvegicus
- plain_language
- Mg exposure can change the amount of the calcium-sensing receptor, adding a slower response to immediate ion sensing.
- primary_references
- [rodriguez-ortiz-2014-pth-context] Magnesium modulates parathyroid hormone secretion and upregulates parathyroid receptor expression at moderately low calcium concentration (2014). https://pubmed.ncbi.nlm.nih.gov/24103811/ DOI: 10.1093/ndt/gft400
- tissue_or_cell_type
- Parathyroid gland
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 289–299
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Six-hour ex-vivo gland incubation with receptor expression assays · source_derived_draft · unverified_draft
### mg-increases-parathyroid-casr-expression At 1.0 mM Ca, six-hour exposure to 2.0 versus 0.5 mM Mg increased CaSR mRNA and protein in intact rat glands. Condition category: normal nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Mg exposure can change the amount of the calcium-sensing receptor, adding a slower response to immediate ion sensing. organism: Rattus norvegicus tissue_or_cell_type: Parathyroid gland experimental_model: Six-hour ex-vivo gland incubation with receptor expression assays limitations: Receptor abundance alone does not prove altered clinical calcium balance; VDR, FGFR1 and Klotho also rose in this experiment. cross_nutrient: magnesium -> calcium sensing [rodriguez-ortiz-2014-pth-context] Magnesium modulates parathyroid hormone secretion and upregulates parathyroid receptor expression at moderately low calcium concentration (2014). https://pubmed.ncbi.nlm.nih.gov/24103811/ DOI: 10.1093/ndt/gft400
Complete structured claim and evidenceFGF23 increases renal distal-tubular TRPV5 membrane abundance through FGFR/alpha-Klotho signaling involving ERK1/2, SGK1 and WNK4.
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
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.