Component
Claudin-2 and claudin-12
Independent biological entity. Read linked claims for experimental scope and context.
2 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
Cldn2/Cldn12 double-null mice lose more urinary calcium than Cldn2-null mice.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- experimental_model
- Cldn2/Cldn12 single/double knockout mice, ex vivo epithelia and cell models
- limitations
- Global deletion also affects intestinal handling.
- nutrient_topic
- Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
- organism
- Mus musculus
- plain_language
- The two claudins provide complementary renal retention.
- primary_references
- [beggs2021] Claudin-2 and claudin-12 form independent, complementary pores required to maintain calcium homeostasis (2021). https://pmc.ncbi.nlm.nih.gov/articles/PMC8694054/ DOI: 10.1073/pnas.2111247118
- tissue_or_cell_type
- Kidney; proximal-tubule localization
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Calcium: mechanism-first literature curation (2026-09-17) · lines 225–234
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cldn2/Cldn12 single/double knockout mice, ex vivo epithelia and cell models · source_derived_draft · unverified_draft
### cldn2-cldn12-double-loss-calciuria Cldn2/Cldn12 double-null mice lose more urinary calcium than Cldn2-null mice. Condition category: machinery_impairment nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The two claudins provide complementary renal retention. organism: Mus musculus tissue_or_cell_type: Kidney; proximal-tubule localization experimental_model: Cldn2/Cldn12 single/double knockout mice, ex vivo epithelia and cell models limitations: Global deletion also affects intestinal handling. [beggs2021] Claudin-2 and claudin-12 form independent, complementary pores required to maintain calcium homeostasis (2021). https://pmc.ncbi.nlm.nih.gov/articles/PMC8694054/ DOI: 10.1073/pnas.2111247118
Complete structured claim and evidenceCldn2/Cldn12 double deletion lowers colonic calcium permeability; small-intestinal permeability was unchanged.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- experimental_model
- Cldn2/Cldn12 single/double knockout mice, ex vivo epithelia and cell models
- limitations
- Global double knockout; single proteins are partly redundant.
- nutrient_topic
- Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
- organism
- Mus musculus
- plain_language
- The measured defect was segment specific.
- primary_references
- [beggs2021] Claudin-2 and claudin-12 form independent, complementary pores required to maintain calcium homeostasis (2021). https://pmc.ncbi.nlm.nih.gov/articles/PMC8694054/ DOI: 10.1073/pnas.2111247118
- tissue_or_cell_type
- Colon
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Calcium: mechanism-first literature curation (2026-09-17) · lines 214–223
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cldn2/Cldn12 single/double knockout mice, ex vivo epithelia and cell models · source_derived_draft · unverified_draft
### cldn2-cldn12-double-loss-colon Cldn2/Cldn12 double deletion lowers colonic calcium permeability; small-intestinal permeability was unchanged. Condition category: machinery_impairment nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The measured defect was segment specific. organism: Mus musculus tissue_or_cell_type: Colon experimental_model: Cldn2/Cldn12 single/double knockout mice, ex vivo epithelia and cell models limitations: Global double knockout; single proteins are partly redundant. [beggs2021] Claudin-2 and claudin-12 form independent, complementary pores required to maintain calcium homeostasis (2021). https://pmc.ncbi.nlm.nih.gov/articles/PMC8694054/ DOI: 10.1073/pnas.2111247118
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.