Component
Claudin-16 RNAi mouse genotype
Transgenic RNAi depletion of mouse claudin-16.
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
Claudin-16 RNAi reduced paracellular cation selectivity in isolated mouse thick ascending limbs.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- TAL electrical selectivity participates in magnesium and calcium conservation; no dietary synergy is implied.
- evidence-system
- Renal RNAi and isolated TAL electrophysiology
- experimental_model
- Renal RNAi and isolated TAL electrophysiology
- limitations
- Selectivity evidence is not proof claudin-16 alone forms a specifically magnesium-selective pore.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Mouse
- plain_language
- The junction lost part of its preference for positively charged ions, changing the conditions that support mineral recovery.
- primary_references
- [hou-2007-cldn16] Transgenic RNAi depletion of claudin-16 and the renal handling of magnesium. (2007). https://pubmed.ncbi.nlm.nih.gov/17442678/ DOI: 10.1074/jbc.M700632200
- tissue
- Renal thick ascending limb
- tissue_or_cell_type
- Renal thick ascending limb
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1097–1109
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Renal RNAi and isolated TAL electrophysiology · source_derived_draft · unverified_draft
### cldn16-depletion-selectivity Claudin-16 RNAi reduced paracellular cation selectivity in isolated mouse thick ascending limbs. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The junction lost part of its preference for positively charged ions, changing the conditions that support mineral recovery. organism: Mouse tissue_or_cell_type: Renal thick ascending limb experimental_model: Renal RNAi and isolated TAL electrophysiology limitations: Selectivity evidence is not proof claudin-16 alone forms a specifically magnesium-selective pore. cross_nutrient: TAL electrical selectivity participates in magnesium and calcium conservation; no dietary synergy is implied. evidence-system: Renal RNAi and isolated TAL electrophysiology tissue: Renal thick ascending limb [hou-2007-cldn16] Transgenic RNAi depletion of claudin-16 and the renal handling of magnesium. (2007). https://pubmed.ncbi.nlm.nih.gov/17442678/ DOI: 10.1074/jbc.M700632200
Complete structured claim and evidenceClaudin-16 RNAi mice developed renal magnesium wasting.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- Calcium wasting accompanied magnesium loss after shared tight-junction impairment.
- evidence-system
- Transgenic Cldn16 RNAi with renal mineral phenotyping
- experimental_model
- Transgenic Cldn16 RNAi with renal mineral phenotyping
- limitations
- This organismal endpoint accompanies selectivity changes; the experiment does not isolate every intervening transport step.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Mouse
- plain_language
- Reducing this tight-junction component made the kidneys lose magnesium.
- primary_references
- [hou-2007-cldn16] Transgenic RNAi depletion of claudin-16 and the renal handling of magnesium. (2007). https://pubmed.ncbi.nlm.nih.gov/17442678/ DOI: 10.1074/jbc.M700632200
- tissue
- Kidney; urine
- tissue_or_cell_type
- Kidney; urine
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1111–1123
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transgenic Cldn16 RNAi with renal mineral phenotyping · source_derived_draft · unverified_draft
### cldn16-rnai-magnesium-loss Claudin-16 RNAi mice developed renal magnesium wasting. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Reducing this tight-junction component made the kidneys lose magnesium. organism: Mouse tissue_or_cell_type: Kidney; urine experimental_model: Transgenic Cldn16 RNAi with renal mineral phenotyping limitations: This organismal endpoint accompanies selectivity changes; the experiment does not isolate every intervening transport step. cross_nutrient: Calcium wasting accompanied magnesium loss after shared tight-junction impairment. evidence-system: Transgenic Cldn16 RNAi with renal mineral phenotyping tissue: Kidney; urine [hou-2007-cldn16] Transgenic RNAi depletion of claudin-16 and the renal handling of magnesium. (2007). https://pubmed.ncbi.nlm.nih.gov/17442678/ DOI: 10.1074/jbc.M700632200
Complete structured claim and evidence
Where it participates (unsigned role)
In the cited RNAi mice, depletion of either claudin-16 or claudin-19 displaced the other from TAL tight junctions.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence-system
- Reciprocal claudin RNAi mouse models and immunolocalization
- experimental_model
- Reciprocal claudin RNAi mouse models and immunolocalization
- limitations
- RNAi-model result; do not universalize junctional interdependence across all knockout backgrounds or human tissue.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Mouse
- plain_language
- The two proteins depended on each other for normal junction placement in these knockdown mice.
- primary_references
- [hou-2009-claudin-assembly] Claudin-16 and claudin-19 interaction is required for their assembly into tight junctions and for renal reabsorption of magnesium (2009). https://pmc.ncbi.nlm.nih.gov/articles/PMC2741254/ DOI: 10.1073/pnas.0907724106
- tissue
- Renal thick ascending limb
- tissue_or_cell_type
- Renal thick ascending limb
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1084–1095
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Reciprocal claudin RNAi mouse models and immunolocalization · source_derived_draft · unverified_draft
### claudin-depletion-displaces-partner In the cited RNAi mice, depletion of either claudin-16 or claudin-19 displaced the other from TAL tight junctions. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The two proteins depended on each other for normal junction placement in these knockdown mice. organism: Mouse tissue_or_cell_type: Renal thick ascending limb experimental_model: Reciprocal claudin RNAi mouse models and immunolocalization limitations: RNAi-model result; do not universalize junctional interdependence across all knockout backgrounds or human tissue. evidence-system: Reciprocal claudin RNAi mouse models and immunolocalization tissue: Renal thick ascending limb [hou-2009-claudin-assembly] Claudin-16 and claudin-19 interaction is required for their assembly into tight junctions and for renal reabsorption of magnesium (2009). https://pmc.ncbi.nlm.nih.gov/articles/PMC2741254/ DOI: 10.1073/pnas.0907724106
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.