Component
CLDN16 loss-of-function genotype
Human pathogenic CLDN16 variants; distinct from mouse RNAi depletion.
1 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 CLDN16 mutations were linked to renal magnesium wasting in the positional-cloning study.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence-system
- Human familial positional genetics and kidney localization
- experimental_model
- Human familial positional genetics and kidney localization
- limitations
- Establishes essential machinery; does not by itself identify a Mg-selective pore.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Human
- plain_language
- A renal tight-junction protein is necessary for the kidney to retain magnesium normally.
- primary_references
- [simon-1999-cldn16] Paracellin-1, a renal tight junction protein required for paracellular Mg2+ resorption (1999). https://pubmed.ncbi.nlm.nih.gov/10390358/ DOI: 10.1126/science.285.5424.103
- 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 1056–1067
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human familial positional genetics and kidney localization · source_derived_draft · unverified_draft
### human-cldn16-magnesium-wasting Human CLDN16 mutations were linked to renal magnesium wasting in the positional-cloning study. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A renal tight-junction protein is necessary for the kidney to retain magnesium normally. organism: Human tissue_or_cell_type: Renal thick ascending limb experimental_model: Human familial positional genetics and kidney localization limitations: Establishes essential machinery; does not by itself identify a Mg-selective pore. evidence-system: Human familial positional genetics and kidney localization tissue: Renal thick ascending limb [simon-1999-cldn16] Paracellin-1, a renal tight junction protein required for paracellular Mg2+ resorption (1999). https://pubmed.ncbi.nlm.nih.gov/10390358/ DOI: 10.1126/science.285.5424.103
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.