Component
Guanosine 5-prime-O-(3-thiotriphosphate)
Poorly hydrolysable GTP analogue used to measure G protein activation.
2 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.
Where it participates (unsigned role)
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.
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 evidenceReconstituted G-protein assays supported Mg-dependent restraint of Galpha nucleotide exchange; reduced Mg enhanced signaling associated with basal CaSR activity.
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
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.