Component
Rat TRPM6
Rat distal-convoluted-tubule magnesium channel. Recorded apart from the human node so a route crossing into it is labelled as orthology.
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 acts on it
Cyclosporine significantly decreased renal expression of the magnesium channel TRPM6 in a rat model of cyclosporine nephrotoxicity.
Experimental context and source evidence
- duration
- Not stated here
- evidence_access
- Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
- experimental_model
- Rat model of cyclosporine nephrotoxicity
- exposure
- Cyclosporine, dose and duration not stated here
- limitations
- Rat expression data. The authors read this as the molecular basis of the renal magnesium loss seen in people given cyclosporine, which is a cross-species interpretation and is recorded as one. Expression is not the same as channel activity.
- organism
- Rat model of cyclosporine nephrotoxicity
- plain_language
- Cyclosporine significantly decreased renal expression of the magnesium channel TRPM6 in a rat model of cyclosporine nephrotoxicity.
- primary_references
- Expression of renal distal tubule transporters TRPM6 and NCC in a rat model of cyclosporine nephrotoxicity and effect of EGF treatment. (2011). https://pubmed.ncbi.nlm.nih.gov/21653632/ DOI: 10.1152/ajprenal.00116.2011
- route
- In vivo
- tissue
- Distal convoluted tubule
Cyclosporine: the complex that inhibits calcineurin, a second cyclophilin, and the transport step that decides exposure (2026-09-23) · lines 223–223
Original AI-assisted curation of seven primary studies resolved by PubMed title search, with every abstract read and all DOIs cross-checked against live PubMed metadata on 2026-09-23. No reference carries a recorded retraction, erratum or expression of concern. Each of the seven is a separate laboratory and each carries its own lineage key, so none of them can be counted twice as independent support. Study-specific concentrations, kinetic constants and limitations retained. Not publisher full text. · supports · Rat model of cyclosporine nephrotoxicity · source_derived_draft · unverified_draft
Cyclosporine significantly decreased renal expression of the magnesium channel TRPM6 in a rat model of cyclosporine nephrotoxicity.
Complete structured claim and evidenceEpidermal growth factor did not raise TRPM6 or lower the fractional excretion of magnesium in cyclosporine-treated rats, although it did both in controls.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- duration
- Not stated here
- evidence_access
- Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
- experimental_model
- Cyclosporine-treated rats compared with controls
- exposure
- Epidermal growth factor administration during cyclosporine treatment
- limitations
- A measured null in the treated arm. It says the EGF route is not simply underfilled during cyclosporine exposure, and it does not say where the block sits.
- organism
- Cyclosporine-treated rats compared with controls
- plain_language
- Epidermal growth factor did not raise TRPM6 or lower the fractional excretion of magnesium in cyclosporine-treated rats, although it did both in controls.
- primary_references
- Expression of renal distal tubule transporters TRPM6 and NCC in a rat model of cyclosporine nephrotoxicity and effect of EGF treatment. (2011). https://pubmed.ncbi.nlm.nih.gov/21653632/ DOI: 10.1152/ajprenal.00116.2011
- route
- In vivo
- tissue
- Distal convoluted tubule
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Cyclosporine: the complex that inhibits calcineurin, a second cyclophilin, and the transport step that decides exposure (2026-09-23) · lines 267–267
Original AI-assisted curation of seven primary studies resolved by PubMed title search, with every abstract read and all DOIs cross-checked against live PubMed metadata on 2026-09-23. No reference carries a recorded retraction, erratum or expression of concern. Each of the seven is a separate laboratory and each carries its own lineage key, so none of them can be counted twice as independent support. Study-specific concentrations, kinetic constants and limitations retained. Not publisher full text. · supports · Cyclosporine-treated rats compared with controls · source_derived_draft · unverified_draft
Epidermal growth factor did not raise TRPM6 or lower the fractional excretion of magnesium in cyclosporine-treated rats, although it did both in controls.
Complete structured claim and evidenceIn control rats given epidermal growth factor, renal TRPM6 expression rose and the fractional excretion of magnesium fell.
Experimental context and source evidence
- duration
- Not stated here
- evidence_access
- Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
- experimental_model
- Control rats
- exposure
- Epidermal growth factor administration
- limitations
- Measured in control animals, which establishes the route without establishing that it is the route cyclosporine breaks.
- organism
- Control rats
- plain_language
- In control rats given epidermal growth factor, renal TRPM6 expression rose and the fractional excretion of magnesium fell.
- primary_references
- Expression of renal distal tubule transporters TRPM6 and NCC in a rat model of cyclosporine nephrotoxicity and effect of EGF treatment. (2011). https://pubmed.ncbi.nlm.nih.gov/21653632/ DOI: 10.1152/ajprenal.00116.2011
- route
- In vivo
- tissue
- Distal convoluted tubule
Cyclosporine: the complex that inhibits calcineurin, a second cyclophilin, and the transport step that decides exposure (2026-09-23) · lines 256–256
Original AI-assisted curation of seven primary studies resolved by PubMed title search, with every abstract read and all DOIs cross-checked against live PubMed metadata on 2026-09-23. No reference carries a recorded retraction, erratum or expression of concern. Each of the seven is a separate laboratory and each carries its own lineage key, so none of them can be counted twice as independent support. Study-specific concentrations, kinetic constants and limitations retained. Not publisher full text. · supports · Control rats · source_derived_draft · unverified_draft
In control rats given epidermal growth factor, renal TRPM6 expression rose and the fractional excretion of magnesium fell.
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.