Component

Ryanodine receptor family / RyR (isoform unspecified)

Ryanodine receptor family / RyR (isoform unspecified). Species, exposure and limitations are retained in each linked claim.

2 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.

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

Where it participates (unsigned role)

  1. Significant inhibition of caffeine-evoked calcium release required 20 µM boric acid in LNCaP cells and 150 µM in non-tumor PWR1E cells.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/boron-research/19554099.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "17bd65bde36f54d1bb0688118212419b31643b9fc61323d12ef1ad6a78a173bb", "start_char": 0, "end_char": 1809, "text_sha256": "17bd65bde36f54d1bb0688118212419b31643b9fc61323d12ef1ad6a78a173bb"}
    experimental_model
    Calcium imaging and flow cytometry in three human prostate cell lines
    exposure
    Boric acid 1–150 µM depending on agonist and cell line; DU-145 storage assay 50 µM for 1 hour
    limitations
    RyR-sensitive flux is not proof of direct binding to a particular RyR isoform. Cell-line exposure responses do not establish dietary prevention of prostate cancer.
    nutrient_topic
    Boron research collection; topical membership is not evidence of a direct dietary effect. · Boron
    organism
    Human DU-145, LNCaP and PWR1E cells
    plain_language
    Different prostate cell types needed different concentrations for the measured response.
    primary_references
    [boron-p19554099] Receptor activated Ca(2+) release is inhibited by boric acid in prostate cancer cells. (2009). https://pubmed.ncbi.nlm.nih.gov/19554099/ DOI: 10.1371/journal.pone.0006009
    tissue_or_cell_type
    Cancer and non-tumor prostate cell cultures

    Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 352–363

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Calcium imaging and flow cytometry in three human prostate cell lines · source_derived_draft · unverified_draft

    ### boron-cell-type-calcium-threshold Significant inhibition of caffeine-evoked calcium release required 20 µM boric acid in LNCaP cells and 150 µM in non-tumor PWR1E cells. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: Different prostate cell types needed different concentrations for the measured response. organism: Human DU-145, LNCaP and PWR1E cells tissue_or_cell_type: Cancer and non-tumor prostate cell cultures experimental_model: Calcium imaging and flow cytometry in three human prostate cell lines limitations: RyR-sensitive flux is not proof of direct binding to a particular RyR isoform. Cell-line exposure responses do not establish dietary prevention of prostate cancer. exposure: Boric acid 1–150 µM depending on agonist and cell line; DU-145 storage assay 50 µM for 1 hour evidence_span: {"source_cache": "artifacts/boron-research/19554099.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "17bd65bde36f54d1bb0688118212419b31643b9fc61323d12ef1ad6a78a173bb", "start_char": 0, "end_char": 1809, "text_sha256": "17bd65bde36f54d1bb0688118212419b31643b9fc61323d12ef1ad6a78a173bb"} [boron-p19554099] Receptor activated Ca(2+) release is inhibited by boric acid in prostate cancer cells. (2009). https://pubmed.ncbi.nlm.nih.gov/19554099/ DOI: 10.1371/journal.pone.0006009
    Complete structured claim and evidence
  2. Boric acid reduced calcium release evoked by ryanodine-receptor agonists in DU-145 cells; cADPR inhibition was detected at 50 µM and responses to other agonists at different concentrations.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/boron-research/19554099.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "17bd65bde36f54d1bb0688118212419b31643b9fc61323d12ef1ad6a78a173bb", "start_char": 0, "end_char": 1809, "text_sha256": "17bd65bde36f54d1bb0688118212419b31643b9fc61323d12ef1ad6a78a173bb"}
    experimental_model
    Calcium imaging and flow cytometry in three human prostate cell lines
    exposure
    Boric acid 1–150 µM depending on agonist and cell line; DU-145 storage assay 50 µM for 1 hour
    limitations
    RyR-sensitive flux is not proof of direct binding to a particular RyR isoform. Cell-line exposure responses do not establish dietary prevention of prostate cancer.
    nutrient_topic
    Boron research collection; topical membership is not evidence of a direct dietary effect. · Boron
    organism
    Human DU-145, LNCaP and PWR1E cells
    plain_language
    Boric acid changed release from a particular calcium store in these cells.
    primary_references
    [boron-p19554099] Receptor activated Ca(2+) release is inhibited by boric acid in prostate cancer cells. (2009). https://pubmed.ncbi.nlm.nih.gov/19554099/ DOI: 10.1371/journal.pone.0006009
    tissue_or_cell_type
    Cancer and non-tumor prostate cell cultures

    Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 326–337

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Calcium imaging and flow cytometry in three human prostate cell lines · source_derived_draft · unverified_draft

    ### boron-ryr-sensitive-calcium Boric acid reduced calcium release evoked by ryanodine-receptor agonists in DU-145 cells; cADPR inhibition was detected at 50 µM and responses to other agonists at different concentrations. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: Boric acid changed release from a particular calcium store in these cells. organism: Human DU-145, LNCaP and PWR1E cells tissue_or_cell_type: Cancer and non-tumor prostate cell cultures experimental_model: Calcium imaging and flow cytometry in three human prostate cell lines limitations: RyR-sensitive flux is not proof of direct binding to a particular RyR isoform. Cell-line exposure responses do not establish dietary prevention of prostate cancer. exposure: Boric acid 1–150 µM depending on agonist and cell line; DU-145 storage assay 50 µM for 1 hour evidence_span: {"source_cache": "artifacts/boron-research/19554099.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "17bd65bde36f54d1bb0688118212419b31643b9fc61323d12ef1ad6a78a173bb", "start_char": 0, "end_char": 1809, "text_sha256": "17bd65bde36f54d1bb0688118212419b31643b9fc61323d12ef1ad6a78a173bb"} [boron-p19554099] Receptor activated Ca(2+) release is inhibited by boric acid in prostate cancer cells. (2009). https://pubmed.ncbi.nlm.nih.gov/19554099/ DOI: 10.1371/journal.pone.0006009
    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