Component
ORAI1
The CRAC channel pore-forming protein.
5 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
ORAI1 supplies the calcium-selective CRAC pore; transmembrane substitutions alter calcium and monovalent-ion permeability.
Experimental context and source evidence
- compartment_description
- Plasma membrane
- experimental_model
- Human ORAI1 mutagenesis and membrane-current/selectivity measurements
- limitations
- Pore evidence does not specify channel stoichiometry or all tissue contributions.
- nutrient_topic
- Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
- organism
- Homo sapiens
- plain_language
- ORAI1 forms the pore through which store-operated calcium enters.
- primary_references
- [ca-prakriya2006] Orai1 is an essential pore subunit of the CRAC channel (2006). https://www.nature.com/articles/nature05122 DOI: 10.1038/nature05122
- research_relationship_category
- transport
- tissue_or_cell_type
- Recombinant channel assays
- transport_effect
- raises The CRAC pore carries calcium from extracellular fluid to cytosol.
- transport_or_reaction_direction
- Extracellular fluid to cytosol
- transport_pool
- cytosolic calcium The CRAC pore carries calcium from extracellular fluid to cytosol.
Calcium: mechanism-first literature curation (2026-09-17) · lines 544–556
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human ORAI1 mutagenesis and membrane-current/selectivity measurements · source_derived_draft · unverified_draft
### ca-orai1-calcium-permeation ORAI1 supplies the calcium-selective CRAC pore; transmembrane substitutions alter calcium and monovalent-ion permeability. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: ORAI1 forms the pore through which store-operated calcium enters. organism: Homo sapiens tissue_or_cell_type: Recombinant channel assays experimental_model: Human ORAI1 mutagenesis and membrane-current/selectivity measurements limitations: Pore evidence does not specify channel stoichiometry or all tissue contributions. research_relationship_category: transport transport_or_reaction_direction: Extracellular fluid to cytosol compartment_description: Plasma membrane [ca-prakriya2006] Orai1 is an essential pore subunit of the CRAC channel (2006). https://www.nature.com/articles/nature05122 DOI: 10.1038/nature05122
Complete structured claim and evidenceHomozygous ORAI1 R91W loss of function abolishes CRAC activity in patient T cells; wild-type ORAI1 restores influx.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- compartment_description
- Plasma membrane
- experimental_model
- Human inherited immune deficiency, patient T-cell rescue and functional channel assays
- limitations
- A rare channelopathy, not nutritional calcium deficiency; the evidence concerns the studied variant.
- nutrient_topic
- Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
- organism
- Homo sapiens
- plain_language
- This inherited channel defect interrupts calcium entry into T cells.
- primary_references
- [ca-feske2006] A mutation in Orai1 causes immune deficiency by abrogating CRAC channel function (2006). https://pubmed.ncbi.nlm.nih.gov/16582901/ DOI: 10.1038/nature04702
- research_relationship_category
- loss_of_function
- tissue_or_cell_type
- Patient T lymphocytes
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Calcium: mechanism-first literature curation (2026-09-17) · lines 558–569
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human inherited immune deficiency, patient T-cell rescue and functional channel assays · source_derived_draft · unverified_draft
### ca-orai1-inherited-loss-influx Homozygous ORAI1 R91W loss of function abolishes CRAC activity in patient T cells; wild-type ORAI1 restores influx. Condition category: machinery_impairment nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This inherited channel defect interrupts calcium entry into T cells. organism: Homo sapiens tissue_or_cell_type: Patient T lymphocytes experimental_model: Human inherited immune deficiency, patient T-cell rescue and functional channel assays limitations: A rare channelopathy, not nutritional calcium deficiency; the evidence concerns the studied variant. research_relationship_category: loss_of_function compartment_description: Plasma membrane [ca-feske2006] A mutation in Orai1 causes immune deficiency by abrogating CRAC channel function (2006). https://pubmed.ncbi.nlm.nih.gov/16582901/ DOI: 10.1038/nature04702
Complete structured claim and evidenceORAI1 enables sustained calcium entry.
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
The cytosolic CRAC-activation domain of STIM1 binds ORAI1 directly and activates its calcium current.
Experimental context and source evidence
- compartment_description
- ER-plasma-membrane junctions
- experimental_model
- Human HEK293/HEK293T expression, electrophysiology and purified protein-binding assays
- limitations
- Domain-expression experiments isolate coupling; physiological amplitude depends on cellular context.
- nutrient_topic
- Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
- organism
- Homo sapiens
- plain_language
- STIM1 directly opens the ORAI1 calcium-entry pathway.
- primary_references
- [ca-park2009] STIM1 clusters and activates CRAC channels via direct binding of a cytosolic domain to Orai1 (2009). https://pubmed.ncbi.nlm.nih.gov/19249086/ DOI: 10.1016/j.cell.2009.02.014
- research_relationship_category
- regulation
- tissue_or_cell_type
- HEK293 expression system and purified proteins
Calcium: mechanism-first literature curation (2026-09-17) · lines 531–542
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human HEK293/HEK293T expression, electrophysiology and purified protein-binding assays · source_derived_draft · unverified_draft
### ca-stim1-direct-orai1-gating The cytosolic CRAC-activation domain of STIM1 binds ORAI1 directly and activates its calcium current. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: STIM1 directly opens the ORAI1 calcium-entry pathway. organism: Homo sapiens tissue_or_cell_type: HEK293 expression system and purified proteins experimental_model: Human HEK293/HEK293T expression, electrophysiology and purified protein-binding assays limitations: Domain-expression experiments isolate coupling; physiological amplitude depends on cellular context. research_relationship_category: regulation compartment_description: ER-plasma-membrane junctions [ca-park2009] STIM1 clusters and activates CRAC channels via direct binding of a cytosolic domain to Orai1 (2009). https://pubmed.ncbi.nlm.nih.gov/19249086/ DOI: 10.1016/j.cell.2009.02.014
Complete structured claim and evidenceOligomerized STIM1 activates ORAI1 and the CRAC channel state.
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.