Component

ORAI1 R91W loss-of-function variant

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

1 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. Homozygous ORAI1 R91W loss of function abolishes CRAC activity in patient T cells; wild-type ORAI1 restores influx.

    ORAI1 → Store-operated calcium entry source_derived_draftungraded
    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 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