Component
CNNM2
Magnesium-homeostasis-associated protein; direct transport versus regulation remains disputed.
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 it acts on
Neither CNNM2 isoform 1 nor isoform 2 produced detectable extra Mg influx or efflux in the reported HEK293 assays.
Experimental context and source evidence
- evidence-system
- Inducible expression, electrophysiology and mag-fura-2 measurements
- experimental_model
- Inducible expression, electrophysiology and mag-fura-2 measurements
- limitations
- A negative expression-system result cannot exclude context-dependent transport or interaction with other machinery.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Human proteins and human-derived cells
- plain_language
- In this experiment, expressing CNNM2 did not behave like adding an independent magnesium transporter.
- primary_references
- [sponder-2016-cnnm2] Human CNNM2 is not a Mg2+ transporter per se (2016). https://pubmed.ncbi.nlm.nih.gov/27068403/ DOI: 10.1007/s00424-016-1816-7
- tissue
- HEK293 culture
- tissue_or_cell_type
- HEK293 culture
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1138–1149
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Inducible expression, electrophysiology and mag-fura-2 measurements · source_derived_draft · unverified_draft
### cnnm2-isoforms-no-extra-mg-flux Neither CNNM2 isoform 1 nor isoform 2 produced detectable extra Mg influx or efflux in the reported HEK293 assays. Condition category: normal nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: In this experiment, expressing CNNM2 did not behave like adding an independent magnesium transporter. organism: Human proteins and human-derived cells tissue_or_cell_type: HEK293 culture experimental_model: Inducible expression, electrophysiology and mag-fura-2 measurements limitations: A negative expression-system result cannot exclude context-dependent transport or interaction with other machinery. evidence-system: Inducible expression, electrophysiology and mag-fura-2 measurements tissue: HEK293 culture [sponder-2016-cnnm2] Human CNNM2 is not a Mg2+ transporter per se (2016). https://pubmed.ncbi.nlm.nih.gov/27068403/ DOI: 10.1007/s00424-016-1816-7
Complete structured claim and evidenceCNNM2 coexpression increased TRPM7-dependent zinc influx, and the TRPM7 E1047K pore mutant prevented this increase.
Experimental context and source evidence
- cross_nutrient
- A protein associated with Mg homeostasis regulates a Zn-permeable channel in culture; nutritional co-dependence was not tested.
- evidence-system
- Coexpression, TRPM7 knockout and pore-inactivation tests
- experimental_model
- Coexpression, TRPM7 knockout and pore-inactivation tests
- limitations
- Zinc is a divalent-flux reporter here; this does not establish CNNM2 as a magnesium pore or dietary Mg-to-Zn dependence.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Human proteins and human-derived cells
- plain_language
- CNNM2 can regulate entry through a separate channel whose pore carries the ion.
- primary_references
- [bai-2021-cnnm-trpm7] CNNM proteins selectively bind to the TRPM7 channel to stimulate divalent cation entry into cells (2021). https://pmc.ncbi.nlm.nih.gov/articles/PMC8726484/ DOI: 10.1371/journal.pbio.3001496
- tissue
- HEK293-family cells; supporting HAP1 cells
- tissue_or_cell_type
- HEK293-family cells; supporting HAP1 cells
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1151–1163
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Coexpression, TRPM7 knockout and pore-inactivation tests · source_derived_draft · unverified_draft
### cnnm2-stimulates-trpm7-zinc-influx CNNM2 coexpression increased TRPM7-dependent zinc influx, and the TRPM7 E1047K pore mutant prevented this increase. Condition category: normal nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: CNNM2 can regulate entry through a separate channel whose pore carries the ion. organism: Human proteins and human-derived cells tissue_or_cell_type: HEK293-family cells; supporting HAP1 cells experimental_model: Coexpression, TRPM7 knockout and pore-inactivation tests limitations: Zinc is a divalent-flux reporter here; this does not establish CNNM2 as a magnesium pore or dietary Mg-to-Zn dependence. cross_nutrient: A protein associated with Mg homeostasis regulates a Zn-permeable channel in culture; nutritional co-dependence was not tested. evidence-system: Coexpression, TRPM7 knockout and pore-inactivation tests tissue: HEK293-family cells; supporting HAP1 cells [bai-2021-cnnm-trpm7] CNNM proteins selectively bind to the TRPM7 channel to stimulate divalent cation entry into cells (2021). https://pmc.ncbi.nlm.nih.gov/articles/PMC8726484/ DOI: 10.1371/journal.pbio.3001496
Complete structured claim and evidence
Where it participates (unsigned role)
CNNM2 variants in the reported families associated with hypomagnesemia, seizures and developmental impairment.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence-system
- Five unrelated families plus functional and zebrafish evidence
- experimental_model
- Five unrelated families plus functional and zebrafish evidence
- limitations
- Neurological features persisted despite supplementation; do not equate the full genetic phenotype with reversible dietary Mg deficiency.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Human
- plain_language
- This inherited disorder includes neurological abnormalities alongside low magnesium.
- primary_references
- [arjona-2014-cnnm2] CNNM2 Mutations Cause Impaired Brain Development and Seizures in Patients with Hypomagnesemia (2014). https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1004267 DOI: 10.1371/journal.pgen.1004267
- tissue
- Kidney and nervous system
- tissue_or_cell_type
- Kidney and nervous system
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1125–1136
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Five unrelated families plus functional and zebrafish evidence · source_derived_draft · unverified_draft
### cnnm2-variants-neurodevelopment CNNM2 variants in the reported families associated with hypomagnesemia, seizures and developmental impairment. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This inherited disorder includes neurological abnormalities alongside low magnesium. organism: Human tissue_or_cell_type: Kidney and nervous system experimental_model: Five unrelated families plus functional and zebrafish evidence limitations: Neurological features persisted despite supplementation; do not equate the full genetic phenotype with reversible dietary Mg deficiency. evidence-system: Five unrelated families plus functional and zebrafish evidence tissue: Kidney and nervous system [arjona-2014-cnnm2] CNNM2 Mutations Cause Impaired Brain Development and Seizures in Patients with Hypomagnesemia (2014). https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1004267 DOI: 10.1371/journal.pgen.1004267
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.