Component
SLC41A1
Mammalian solute carrier linked experimentally to Mg2+ efflux; coupling and organismal importance depend on model.
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
Human SLC41A1-associated Mg efflux in HEK293 cells fell sharply when extracellular sodium was replaced in the Kolisek assay.
Experimental context and source evidence
- cross_nutrient
- Sodium availability affected measured magnesium export in this assay; coupling is contested.
- evidence-system
- Human construct overexpression; mag-fura-2; extracellular Na replacement
- experimental_model
- Human construct overexpression; mag-fura-2; extracellular Na replacement
- limitations
- Indirect free-ion assay and overexpression; conflicts with sodium-independent isotope flux in a different construct/protocol.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Human protein and human-derived cells
- plain_language
- This experiment supported sodium-coupled export of magnesium.
- primary_references
- [kolisek-2012-slc41a1] Human gene SLC41A1 encodes for the Na+/Mg2+ exchanger (2012). https://pubmed.ncbi.nlm.nih.gov/22031603/ DOI: 10.1152/ajpcell.00289.2011
- tissue
- HEK293 cells
- tissue_or_cell_type
- HEK293 cells
- transport_direction
- Mg2+ from cytosol toward extracellular solution.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1165–1178
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human construct overexpression; mag-fura-2; extracellular Na replacement · source_derived_draft · unverified_draft
### slc41a1-sodium-dependent-efflux Human SLC41A1-associated Mg efflux in HEK293 cells fell sharply when extracellular sodium was replaced in the Kolisek assay. Condition category: normal nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This experiment supported sodium-coupled export of magnesium. organism: Human protein and human-derived cells tissue_or_cell_type: HEK293 cells experimental_model: Human construct overexpression; mag-fura-2; extracellular Na replacement limitations: Indirect free-ion assay and overexpression; conflicts with sodium-independent isotope flux in a different construct/protocol. cross_nutrient: Sodium availability affected measured magnesium export in this assay; coupling is contested. transport_direction: Mg2+ from cytosol toward extracellular solution. evidence-system: Human construct overexpression; mag-fura-2; extracellular Na replacement tissue: HEK293 cells [kolisek-2012-slc41a1] Human gene SLC41A1 encodes for the Na+/Mg2+ exchanger (2012). https://pubmed.ncbi.nlm.nih.gov/22031603/ DOI: 10.1152/ajpcell.00289.2011
Complete structured claim and evidenceMouse SLC41A1 expressed in HEK293 cells supported Mg extrusion without extracellular sodium in the Arjona isotope assay.
Experimental context and source evidence
- cross_nutrient
- This assay challenges obligatory sodium dependence of SLC41A1-associated magnesium extrusion.
- evidence-system
- Mouse SLC41A1 construct; stable-isotope 25Mg measurements
- experimental_model
- Mouse SLC41A1 construct; stable-isotope 25Mg measurements
- limitations
- Different ortholog, loading and readout from the sodium-dependent report; physiological coupling remains unresolved.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Mouse protein; human-derived cells
- plain_language
- A different experiment found magnesium export that did not require sodium.
- primary_references
- [arjona-2019-slc41a1] SLC41A1 is essential for magnesium homeostasis in vivo (2019). https://pubmed.ncbi.nlm.nih.gov/30417250/ DOI: 10.1007/s00424-018-2234-9
- tissue
- HEK293 cells
- tissue_or_cell_type
- HEK293 cells
- transport_direction
- Mg2+ from cytosol toward extracellular solution.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1180–1193
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse SLC41A1 construct; stable-isotope 25Mg measurements · source_derived_draft · unverified_draft
### slc41a1-sodium-independent-efflux Mouse SLC41A1 expressed in HEK293 cells supported Mg extrusion without extracellular sodium in the Arjona isotope assay. Condition category: normal nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A different experiment found magnesium export that did not require sodium. organism: Mouse protein; human-derived cells tissue_or_cell_type: HEK293 cells experimental_model: Mouse SLC41A1 construct; stable-isotope 25Mg measurements limitations: Different ortholog, loading and readout from the sodium-dependent report; physiological coupling remains unresolved. cross_nutrient: This assay challenges obligatory sodium dependence of SLC41A1-associated magnesium extrusion. transport_direction: Mg2+ from cytosol toward extracellular solution. evidence-system: Mouse SLC41A1 construct; stable-isotope 25Mg measurements tissue: HEK293 cells [arjona-2019-slc41a1] SLC41A1 is essential for magnesium homeostasis in vivo (2019). https://pubmed.ncbi.nlm.nih.gov/30417250/ DOI: 10.1007/s00424-018-2234-9
Complete structured claim and evidence
Where it participates (unsigned role)
Slc41a1-null mice maintained serum and urinary Mg similarly to littermates under standard and Mg-restricted diets.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence-system
- Constitutive knockout with dietary Mg restriction challenge
- experimental_model
- Constitutive knockout with dietary Mg restriction challenge
- limitations
- Does not prove absence of all cell-specific functions; zebrafish and overexpression findings have different scope.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Mouse
- plain_language
- Deleting SLC41A1 did not make these mice uniquely unable to maintain magnesium balance.
- primary_references
- [ilenwabor-2022-slc41a1] SLC41A1 knockout mice display normal magnesium homeostasis (2022). https://pubmed.ncbi.nlm.nih.gov/36049064/ DOI: 10.1152/ajprenal.00101.2022
- tissue
- Kidney; serum and urine
- tissue_or_cell_type
- Kidney; serum and urine
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1195–1206
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Constitutive knockout with dietary Mg restriction challenge · source_derived_draft · unverified_draft
### slc41a1-null-mouse-magnesium-preserved Slc41a1-null mice maintained serum and urinary Mg similarly to littermates under standard and Mg-restricted diets. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Deleting SLC41A1 did not make these mice uniquely unable to maintain magnesium balance. organism: Mouse tissue_or_cell_type: Kidney; serum and urine experimental_model: Constitutive knockout with dietary Mg restriction challenge limitations: Does not prove absence of all cell-specific functions; zebrafish and overexpression findings have different scope. evidence-system: Constitutive knockout with dietary Mg restriction challenge tissue: Kidney; serum and urine [ilenwabor-2022-slc41a1] SLC41A1 knockout mice display normal magnesium homeostasis (2022). https://pubmed.ncbi.nlm.nih.gov/36049064/ DOI: 10.1152/ajprenal.00101.2022
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.