Component
ER calcium release
Release of calcium through functional IP3R channels.
4 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
ER calcium release causes store depletion.
Experimental context and source evidence
- cell_type
- · T cell
- evidence_scope
- Source-derived draft; primary-source verification required
- organism
- · Human
Selenium in immune cells · lines 30–38
Selenium immune-cell mechanism draft · supports · Source draft; model details require primary-source verification · source_derived_draft · unverified_draft
5. TCR → LCK → ZAP70 → LAT → PLCγ1 → PIP₂ → IP₃ + DAG 6. IP₃ → IP3R → ER Ca²⁺ release → store depletion 7. STIM1 oligomerizes → ORAI1 → CRAC channel → sustained Ca²⁺ entry 8. Ca²⁺/calmodulin → CALCINEURIN (PP2B) → dephosphorylates NFAT 9. NFAT → nucleus → partners with AP-1 → IL2, IFNG, CD25 transcription
Complete structured claim and evidence
What acts on it
Applied IP3 releases calcium from a nonmitochondrial intracellular store in permeabilized pancreatic acinar cells.
Experimental context and source evidence
- compartment_description
- Nonmitochondrial intracellular store to cytosol
- experimental_model
- Permeabilized rat pancreatic acinar cells
- limitations
- Permeabilized-cell application; receptor isoform and dietary status were not established.
- nutrient_topic
- Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
- organism
- Rattus norvegicus
- plain_language
- IP3 releases stored calcium inside acinar cells.
- primary_references
- [ca-streb1983] Release of Ca2+ from a nonmitochondrial intracellular store in pancreatic acinar cells by inositol-1,4,5-trisphosphate (1983). https://pubmed.ncbi.nlm.nih.gov/6605482/ DOI: 10.1038/306067a0
- research_relationship_category
- mechanism
- tissue_or_cell_type
- Pancreatic acinar cells
- transport_or_reaction_direction
- Intracellular store to cytosol
Calcium: mechanism-first literature curation (2026-09-17) · lines 464–476
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Permeabilized rat pancreatic acinar cells · source_derived_draft · unverified_draft
### ca-ip3-mobilizes-store Applied IP3 releases calcium from a nonmitochondrial intracellular store in permeabilized pancreatic acinar cells. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: IP3 releases stored calcium inside acinar cells. organism: Rattus norvegicus tissue_or_cell_type: Pancreatic acinar cells experimental_model: Permeabilized rat pancreatic acinar cells limitations: Permeabilized-cell application; receptor isoform and dietary status were not established. research_relationship_category: mechanism transport_or_reaction_direction: Intracellular store to cytosol compartment_description: Nonmitochondrial intracellular store to cytosol [ca-streb1983] Release of Ca2+ from a nonmitochondrial intracellular store in pancreatic acinar cells by inositol-1,4,5-trisphosphate (1983). https://pubmed.ncbi.nlm.nih.gov/6605482/ DOI: 10.1038/306067a0
Complete structured claim and evidenceSELENOK-null mice show blunted immune-cell calcium flux in the source-described IP3R-dependent ER calcium-release pathway.
Experimental context and source evidence
- availability_state
- Insufficient or absent SELENOK function; the reported phenotype comes from SELENOK-null mice.
- experimental_scope
- SELENOK loss-of-function animal model and supplied biochemical mechanism, including T-cell context.
- limitations
- Dietary selenium restriction is not proven equivalent to SELENOK knockout. No selenium concentration is mapped to this phenotype, and this scenario does not invert every downstream normal-path arrow.
- trigger_kind
- machinery_impairment
Selenium in immune cells · lines 27–32
Selenium immune-cell mechanism draft · supports · Supplied reference; verify the primary study and experimental context. · source_derived_draft · unverified_draft
4. Palmitoylated IP3R = stable, correctly localized, functional channel Non-palmitoylated IP3R = degraded / non-functional 5. TCR → LCK → ZAP70 → LAT → PLCγ1 → PIP₂ → IP₃ + DAG 6. IP₃ → IP3R → ER Ca²⁺ release → store depletion
Selenium in immune cells · lines 42–42
Selenium immune-cell mechanism draft · supports · Supplied reference; verify the primary study and experimental context. · source_derived_draft · unverified_draft
**Kill SELENOK and you lose step 4.** The phenotype in SELENOK⁻/⁻ mice is exactly what the chain predicts: blunted Ca²⁺ flux in **T cells, B cells, neutrophils, and macrophages**; reduced TCR-driven proliferation; impaired chemotaxis; reduced IL-2.
Complete structured claim and evidenceFunctional IP3R enables release of calcium from the ER.
Experimental context and source evidence
- cell_type
- · T cell
- evidence_scope
- Source-derived draft; primary-source verification required
- organism
- · Human
Selenium in immune cells · lines 30–38
Selenium immune-cell mechanism draft · supports · Source draft; model details require primary-source verification · source_derived_draft · unverified_draft
5. TCR → LCK → ZAP70 → LAT → PLCγ1 → PIP₂ → IP₃ + DAG 6. IP₃ → IP3R → ER Ca²⁺ release → store depletion 7. STIM1 oligomerizes → ORAI1 → CRAC channel → sustained Ca²⁺ entry 8. Ca²⁺/calmodulin → CALCINEURIN (PP2B) → dephosphorylates NFAT 9. NFAT → nucleus → partners with AP-1 → IL2, IFNG, CD25 transcription
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.