Component

G protein alpha-i1 subunit / GNAI1

Galpha-i1 protein identified in the primary methods. The assayed recombinant preparation contained an internal hexahistidine tag after residue 121 and was expressed in E. coli; source species of the cDNA is not assigned here.

2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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. The low-Mg enhancement of CaSR-stimulated GTP analogue binding was lost with the reduced-Mg-sensitivity Galpha-i1 R209C mutant; changing receptor extracellular cation affinity did not remove it.

    GNAI1 R209C experimental mutant → G protein alpha guanine-nucleotide exchange source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    magnesium -> CaSR/PTH -> calcium
    experimental_model
    Engineered receptor and Galpha comparison in reconstituted signaling assays
    limitations
    Engineered mutant evidence is separate from nutrient deficiency; no claim that R209C occurs in affected patients or that every receptor mechanism is excluded.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Human CaSR expression system; engineered G-protein preparation
    plain_language
    The mutant experiments placed this Mg effect at the G-protein switch rather than simply at the receptor surface where calcium and magnesium bind.
    primary_references
    [quitterer-2001-magnesium-paradox] Paradoxical block of parathormone secretion is mediated by increased activity of G alpha subunits (2001). https://pubmed.ncbi.nlm.nih.gov/11102444/ DOI: 10.1074/jbc.M007727200
    tissue_or_cell_type
    HEK-293 membrane reconstitution
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 469–479

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Engineered receptor and Galpha comparison in reconstituted signaling assays · source_derived_draft · unverified_draft

    ### galpha-r209c-removes-magnesium-dependence The low-Mg enhancement of CaSR-stimulated GTP analogue binding was lost with the reduced-Mg-sensitivity Galpha-i1 R209C mutant; changing receptor extracellular cation affinity did not remove it. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The mutant experiments placed this Mg effect at the G-protein switch rather than simply at the receptor surface where calcium and magnesium bind. organism: Human CaSR expression system; engineered G-protein preparation tissue_or_cell_type: HEK-293 membrane reconstitution experimental_model: Engineered receptor and Galpha comparison in reconstituted signaling assays limitations: Engineered mutant evidence is separate from nutrient deficiency; no claim that R209C occurs in affected patients or that every receptor mechanism is excluded. cross_nutrient: magnesium -> CaSR/PTH -> calcium [quitterer-2001-magnesium-paradox] Paradoxical block of parathormone secretion is mediated by increased activity of G alpha subunits (2001). https://pubmed.ncbi.nlm.nih.gov/11102444/ DOI: 10.1074/jbc.M007727200
    Complete structured claim and evidence

  2. Reconstituted G-protein assays supported Mg-dependent restraint of Galpha nucleotide exchange; reduced Mg enhanced signaling associated with basal CaSR activity.

    Mg2+ → G protein alpha guanine-nucleotide exchange source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    magnesium -> CaSR/PTH -> calcium
    experimental_model
    CaSR-expressing HEK-293 membranes reconstituted with G proteins
    limitations
    Mechanistic explanation supported by probes; not an established sole cause of human hypomagnesemic hypocalcemia.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Human receptor-expression system with purified/recombinant G proteins
    plain_language
    Less Mg can loosen the restraint on the G-protein switch, allowing the receptor pathway to suppress PTH more strongly.
    primary_references
    [quitterer-2001-magnesium-paradox] Paradoxical block of parathormone secretion is mediated by increased activity of G alpha subunits (2001). https://pubmed.ncbi.nlm.nih.gov/11102444/ DOI: 10.1074/jbc.M007727200
    tissue_or_cell_type
    Reconstituted membrane signaling system
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 457–467

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · CaSR-expressing HEK-293 membranes reconstituted with G proteins · source_derived_draft · unverified_draft

    ### low-mg-galpha-exchange-explains-paradox Reconstituted G-protein assays supported Mg-dependent restraint of Galpha nucleotide exchange; reduced Mg enhanced signaling associated with basal CaSR activity. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Less Mg can loosen the restraint on the G-protein switch, allowing the receptor pathway to suppress PTH more strongly. organism: Human receptor-expression system with purified/recombinant G proteins tissue_or_cell_type: Reconstituted membrane signaling system experimental_model: CaSR-expressing HEK-293 membranes reconstituted with G proteins limitations: Mechanistic explanation supported by probes; not an established sole cause of human hypomagnesemic hypocalcemia. cross_nutrient: magnesium -> CaSR/PTH -> calcium [quitterer-2001-magnesium-paradox] Paradoxical block of parathormone secretion is mediated by increased activity of G alpha subunits (2001). https://pubmed.ncbi.nlm.nih.gov/11102444/ DOI: 10.1074/jbc.M007727200
    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