Component

Fibroblast growth factor receptor 1 / FGFR1

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

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 acts on it

  1. Alpha-Klotho cooperates with FGFR1(IIIc) to confer high-affinity binding and signaling by FGF23.

    Alpha-Klotho / KL → Fibroblast growth factor receptor 1 / FGFR1 source_derived_draftungraded
    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

  2. FGFR1 oxidation promoted receptor activation and downstream signaling in the phosphate-sensing tumor-model experiments.

    FGFR1 cysteine/methionine oxidation in the 2026 osteosarcoma study → Fibroblast growth factor receptor 1 / FGFR1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/phosphorus-research/42247296.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a8d4221d8a5c56a5937ab8262e3ece5ed87692cb876ddcc0a08e7f68b66a9b76", "start_char": 0, "end_char": 1041, "text_sha256": "a8d4221d8a5c56a5937ab8262e3ece5ed87692cb876ddcc0a08e7f68b66a9b76"}
    experimental_model
    Osteosarcoma-cell signaling with in-vivo tumor experiments
    exposure
    Elevated phosphate challenges and receptor activation experiments
    limitations
    New 2026 mechanism in tumor models; blood-Pi/tumor-growth association is not proof that dietary phosphorus causes human cancer. No specific transporter or oxidized residue number is invented from the abstract.
    nutrient_topic
    Phosphorus research collection; topical membership is not evidence of a direct dietary effect. · Phosphorus
    organism
    Osteosarcoma cellular and animal systems; precise species not fully resolved from abstract
    plain_language
    Phosphate triggered receptor signaling through an indirect chemical route.
    primary_references
    [phosphorus-p42247296] Unconventional activation of the proto-oncogene FGFR1 by extracellular phosphate via H2O2-mediated kinase oxidation. (2026). https://pubmed.ncbi.nlm.nih.gov/42247296/ DOI: 10.1016/j.celrep.2026.117504
    tissue_or_cell_type
    Plasma-membrane/mitochondrial phosphate handling and FGFR1 signaling

    Phosphorus: metabolism, signaling and nutrient connections (2026-09-17) · lines 893–904

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Osteosarcoma-cell signaling with in-vivo tumor experiments · source_derived_draft · unverified_draft

    ### phosphorus-fgfr-activation FGFR1 oxidation promoted receptor activation and downstream signaling in the phosphate-sensing tumor-model experiments. Condition category: normal nutrient_topic: Phosphorus research collection; topical membership is not evidence of a direct dietary effect. plain_language: Phosphate triggered receptor signaling through an indirect chemical route. organism: Osteosarcoma cellular and animal systems; precise species not fully resolved from abstract tissue_or_cell_type: Plasma-membrane/mitochondrial phosphate handling and FGFR1 signaling experimental_model: Osteosarcoma-cell signaling with in-vivo tumor experiments limitations: New 2026 mechanism in tumor models; blood-Pi/tumor-growth association is not proof that dietary phosphorus causes human cancer. No specific transporter or oxidized residue number is invented from the abstract. exposure: Elevated phosphate challenges and receptor activation experiments evidence_span: {"source_cache": "artifacts/phosphorus-research/42247296.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a8d4221d8a5c56a5937ab8262e3ece5ed87692cb876ddcc0a08e7f68b66a9b76", "start_char": 0, "end_char": 1041, "text_sha256": "a8d4221d8a5c56a5937ab8262e3ece5ed87692cb876ddcc0a08e7f68b66a9b76"} [phosphorus-p42247296] Unconventional activation of the proto-oncogene FGFR1 by extracellular phosphate via H2O2-mediated kinase oxidation. (2026). https://pubmed.ncbi.nlm.nih.gov/42247296/ DOI: 10.1016/j.celrep.2026.117504
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. 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.

    Mg2+ → Calcium-sensing receptor / CaSR source_derived_draftungraded
    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 evidence

  2. The phosphate-associated hydrogen-peroxide burst oxidized critical cysteine and methionine residues of FGFR1.

    Hydrogen peroxide → FGFR1 cysteine/methionine oxidation in the 2026 osteosarcoma study source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/phosphorus-research/42247296.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a8d4221d8a5c56a5937ab8262e3ece5ed87692cb876ddcc0a08e7f68b66a9b76", "start_char": 0, "end_char": 1041, "text_sha256": "a8d4221d8a5c56a5937ab8262e3ece5ed87692cb876ddcc0a08e7f68b66a9b76"}
    experimental_model
    Osteosarcoma-cell signaling with in-vivo tumor experiments
    exposure
    Elevated phosphate challenges and receptor activation experiments
    limitations
    New 2026 mechanism in tumor models; blood-Pi/tumor-growth association is not proof that dietary phosphorus causes human cancer. No specific transporter or oxidized residue number is invented from the abstract.
    nutrient_topic
    Phosphorus research collection; topical membership is not evidence of a direct dietary effect. · Phosphorus
    organism
    Osteosarcoma cellular and animal systems; precise species not fully resolved from abstract
    plain_language
    A redox change reached the receptor protein.
    primary_references
    [phosphorus-p42247296] Unconventional activation of the proto-oncogene FGFR1 by extracellular phosphate via H2O2-mediated kinase oxidation. (2026). https://pubmed.ncbi.nlm.nih.gov/42247296/ DOI: 10.1016/j.celrep.2026.117504
    tissue_or_cell_type
    Plasma-membrane/mitochondrial phosphate handling and FGFR1 signaling

    Phosphorus: metabolism, signaling and nutrient connections (2026-09-17) · lines 880–891

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Osteosarcoma-cell signaling with in-vivo tumor experiments · source_derived_draft · unverified_draft

    ### phosphorus-peroxide-fgfr The phosphate-associated hydrogen-peroxide burst oxidized critical cysteine and methionine residues of FGFR1. Condition category: normal nutrient_topic: Phosphorus research collection; topical membership is not evidence of a direct dietary effect. plain_language: A redox change reached the receptor protein. organism: Osteosarcoma cellular and animal systems; precise species not fully resolved from abstract tissue_or_cell_type: Plasma-membrane/mitochondrial phosphate handling and FGFR1 signaling experimental_model: Osteosarcoma-cell signaling with in-vivo tumor experiments limitations: New 2026 mechanism in tumor models; blood-Pi/tumor-growth association is not proof that dietary phosphorus causes human cancer. No specific transporter or oxidized residue number is invented from the abstract. exposure: Elevated phosphate challenges and receptor activation experiments evidence_span: {"source_cache": "artifacts/phosphorus-research/42247296.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a8d4221d8a5c56a5937ab8262e3ece5ed87692cb876ddcc0a08e7f68b66a9b76", "start_char": 0, "end_char": 1041, "text_sha256": "a8d4221d8a5c56a5937ab8262e3ece5ed87692cb876ddcc0a08e7f68b66a9b76"} [phosphorus-p42247296] Unconventional activation of the proto-oncogene FGFR1 by extracellular phosphate via H2O2-mediated kinase oxidation. (2026). https://pubmed.ncbi.nlm.nih.gov/42247296/ DOI: 10.1016/j.celrep.2026.117504
    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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