Component
Store-operated calcium entry
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 acts on it
Homozygous 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 evidenceSTIM1 knockdown suppresses store-depletion-triggered calcium influx in HeLa cells.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- compartment_description
- ER-plasma-membrane signaling junction
- experimental_model
- Human HeLa cells; RNA interference screen, calcium imaging and STIM1 EF-hand mutagenesis
- limitations
- RNA interference perturbs signaling machinery; it does not model low calcium intake.
- nutrient_topic
- Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
- organism
- Homo sapiens
- plain_language
- Reducing STIM1 weakens calcium entry after stores empty.
- primary_references
- [ca-liou2005] STIM is a Ca2+ sensor essential for Ca2+-store-depletion-triggered Ca2+ influx (2005). https://pubmed.ncbi.nlm.nih.gov/16005298/ DOI: 10.1016/j.cub.2005.05.055
- research_relationship_category
- loss_of_function
- tissue_or_cell_type
- HeLa cells
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Calcium: mechanism-first literature curation (2026-09-17) · lines 518–529
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human HeLa cells; RNA interference screen, calcium imaging and STIM1 EF-hand mutagenesis · source_derived_draft · unverified_draft
### ca-stim1-knockdown-influx STIM1 knockdown suppresses store-depletion-triggered calcium influx in HeLa cells. Condition category: machinery_impairment nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Reducing STIM1 weakens calcium entry after stores empty. organism: Homo sapiens tissue_or_cell_type: HeLa cells experimental_model: Human HeLa cells; RNA interference screen, calcium imaging and STIM1 EF-hand mutagenesis limitations: RNA interference perturbs signaling machinery; it does not model low calcium intake. research_relationship_category: loss_of_function compartment_description: ER-plasma-membrane signaling junction [ca-liou2005] STIM is a Ca2+ sensor essential for Ca2+-store-depletion-triggered Ca2+ influx (2005). https://pubmed.ncbi.nlm.nih.gov/16005298/ DOI: 10.1016/j.cub.2005.05.055
Complete structured claim and evidence
Where it participates (unsigned role)
DIM increased STIM1 expression and supported store-operated calcium entry in the experimental muscle model.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/dim-research/42308990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4bd26fd33c370df293346c5680820459a885a7545286d92c9e1c27220d41f2cb", "start_char": 0, "end_char": 2803, "text_sha256": "4bd26fd33c370df293346c5680820459a885a7545286d92c9e1c27220d41f2cb"}
- experimental_model
- Dexamethasone atrophy and aging-model experiments
- exposure
- DIM in experimental atrophy/aging models
- limitations
- 2026 preclinical study, not a human sarcopenia trial. Mouse STIM1 stays distinct from the human selenium-linked STIM1 record.
- nutrient_topic
- Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. · 3,3'-Diindolylmethane / DIM
- organism
- Mouse muscle, mouse C2C12 myotubes and C. elegans
- plain_language
- Calcium signaling is another network connection, with species kept explicit.
- primary_references
- [dim-p42308990] 3,3'-Diindolylmethane ameliorates muscle atrophy by modulating mitochondrial function and calcium homeostasis. (2026). https://pubmed.ncbi.nlm.nih.gov/42308990/ DOI: 10.1016/j.phymed.2026.158409
- tissue_or_cell_type
- Mitochondrial function and store-operated calcium entry
Diindolylmethane (DIM): formation, receptor signaling, metabolism and drug interactions (2026-09-17) · lines 1455–1466
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dexamethasone atrophy and aging-model experiments · source_derived_draft · unverified_draft
### dim-mouse-stim1 DIM increased STIM1 expression and supported store-operated calcium entry in the experimental muscle model. Condition category: normal nutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Calcium signaling is another network connection, with species kept explicit. organism: Mouse muscle, mouse C2C12 myotubes and C. elegans tissue_or_cell_type: Mitochondrial function and store-operated calcium entry experimental_model: Dexamethasone atrophy and aging-model experiments limitations: 2026 preclinical study, not a human sarcopenia trial. Mouse STIM1 stays distinct from the human selenium-linked STIM1 record. exposure: DIM in experimental atrophy/aging models evidence_span: {"source_cache": "artifacts/dim-research/42308990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4bd26fd33c370df293346c5680820459a885a7545286d92c9e1c27220d41f2cb", "start_char": 0, "end_char": 2803, "text_sha256": "4bd26fd33c370df293346c5680820459a885a7545286d92c9e1c27220d41f2cb"} [dim-p42308990] 3,3'-Diindolylmethane ameliorates muscle atrophy by modulating mitochondrial function and calcium homeostasis. (2026). https://pubmed.ncbi.nlm.nih.gov/42308990/ DOI: 10.1016/j.phymed.2026.158409
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.