Component
Pertussis toxin
Experimental inhibitor of Gi/o signaling used to test pathway participation.
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.
What it acts on
Pertussis-toxin pretreatment abolished the suppression of PTH release by low Mg in the parathyroid-cell assay.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- magnesium -> CaSR/PTH -> calcium
- experimental_model
- Dispersed human parathyroid cells from hyperparathyroid tissue
- limitations
- Pharmacologic pathway probe, not evidence for toxin use in patients; no full in-vivo chain tested.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Homo sapiens
- plain_language
- Blocking Gi/o signaling removed the low-Mg secretory brake, placing these signaling proteins in the experimental pathway.
- 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
- Parathyroid cells in vitro
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 445–455
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dispersed human parathyroid cells from hyperparathyroid tissue · source_derived_draft · unverified_draft
### pertussis-toxin-removes-low-mg-pth-block Pertussis-toxin pretreatment abolished the suppression of PTH release by low Mg in the parathyroid-cell assay. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blocking Gi/o signaling removed the low-Mg secretory brake, placing these signaling proteins in the experimental pathway. organism: Homo sapiens tissue_or_cell_type: Parathyroid cells in vitro experimental_model: Dispersed human parathyroid cells from hyperparathyroid tissue limitations: Pharmacologic pathway probe, not evidence for toxin use in patients; no full in-vivo chain tested. 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
Where it participates (unsigned role)
A cloned complementary DNA encoded a G protein-coupled receptor that inhibits adenylate cyclase in a dose-dependent, stereoselective and pertussis-toxin-sensitive manner, is more responsive to psychoactive than to non-psychoactive cannabinoids, and whose messenger RNA is found in the brain regions that have cannabinoid receptors.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/thc-research/2165569.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8d92b7104006ccc194ab498aa8f559606353e6ccc4b5aa7af0a9502c9bfc37db", "start_char": 0, "end_char": 1256, "text_sha256": "8d92b7104006ccc194ab498aa8f559606353e6ccc4b5aa7af0a9502c9bfc37db"}
- experimental_model
- Cloning and heterologous expression of a complementary DNA from rat brain
- exposure
- Cannabinoid binding and adenylate cyclase inhibition in the transfected cells
- limitations
- The founding cloning paper. It establishes a receptor, which is what displaced the membrane-disruption explanation of cannabinoid action.
- nutrient_topic
- THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. · Delta-9-tetrahydrocannabinol / THC
- organism
- Rat receptor expressed in cells
- plain_language
- Cannabis acts on a specific receptor, not by melting cell membranes as was assumed.
- primary_references
- [thc-p2165569] Structure of a cannabinoid receptor and functional expression of the cloned cDNA. (1990). https://pubmed.ncbi.nlm.nih.gov/2165569/ DOI: 10.1038/346561a0
- tissue_or_cell_type
- Brain and neural cell lines
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cloning and heterologous expression of a complementary DNA from rat brain · source_derived_draft · unverified_draft
### thc-cb1-cloned A cloned complementary DNA encoded a G protein-coupled receptor that inhibits adenylate cyclase in a dose-dependent, stereoselective and pertussis-toxin-sensitive manner, is more responsive to psychoactive than to non-psychoactive cannabinoids, and whose messenger RNA is found in the brain regions that have cannabinoid receptors. Condition category: normal nutrient_topic: THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. plain_language: Cannabis acts on a specific receptor, not by melting cell membranes as was assumed. organism: Rat receptor expressed in cells tissue_or_cell_type: Brain and neural cell lines experimental_model: Cloning and heterologous expression of a complementary DNA from rat brain limitations: The founding cloning paper. It establishes a receptor, which is what displaced the membrane-disruption explanation of cannabinoid action. exposure: Cannabinoid binding and adenylate cyclase inhibition in the transfected cells evidence_span: {"source_cache": "artifacts/thc-research/2165569.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8d92b7104006ccc194ab498aa8f559606353e6ccc4b5aa7af0a9502c9bfc37db", "start_char": 0, "end_char": 1256, "text_sha256": "8d92b7104006ccc194ab498aa8f559606353e6ccc4b5aa7af0a9502c9bfc37db"} [thc-p2165569] Structure of a cannabinoid receptor and functional expression of the cloned cDNA. (1990). https://pubmed.ncbi.nlm.nih.gov/2165569/ DOI: 10.1038/346561a0
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.