Component
Intestine-specific Trpm7-null mouse genotype
Villin1-Cre conditional mouse Trpm7 deletion.
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
Intestinal Trpm7 deletion reduced serum and bone calcium in suckling mice.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- TRPM7 is shared machinery for magnesium and calcium handling in this developmental model; causal Mg-to-Ca nutritional dependence was not isolated.
- evidence-system
- Conditional knockout; postnatal mineral phenotyping
- experimental_model
- Conditional knockout; postnatal mineral phenotyping
- limitations
- Shared channel loss; does not prove low Mg intake causes calcium malabsorption.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Mouse
- plain_language
- The same epithelial channel machinery supports calcium as well as magnesium supply.
- primary_references
- [mittermeier-2019-trpm7] TRPM7 is the central gatekeeper of intestinal mineral absorption essential for postnatal survival (2019). https://pubmed.ncbi.nlm.nih.gov/30770447/ DOI: 10.1073/pnas.1810633116
- tissue
- Intestine; serum and bone
- tissue_or_cell_type
- Intestine; serum and bone
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 988–1000
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Conditional knockout; postnatal mineral phenotyping · source_derived_draft · unverified_draft
### intestinal-trpm7-loss-calcium Intestinal Trpm7 deletion reduced serum and bone calcium in suckling mice. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The same epithelial channel machinery supports calcium as well as magnesium supply. organism: Mouse tissue_or_cell_type: Intestine; serum and bone experimental_model: Conditional knockout; postnatal mineral phenotyping limitations: Shared channel loss; does not prove low Mg intake causes calcium malabsorption. cross_nutrient: TRPM7 is shared machinery for magnesium and calcium handling in this developmental model; causal Mg-to-Ca nutritional dependence was not isolated. evidence-system: Conditional knockout; postnatal mineral phenotyping tissue: Intestine; serum and bone [mittermeier-2019-trpm7] TRPM7 is the central gatekeeper of intestinal mineral absorption essential for postnatal survival (2019). https://pubmed.ncbi.nlm.nih.gov/30770447/ DOI: 10.1073/pnas.1810633116
Complete structured claim and evidenceIntestinal Trpm7 deletion lowered magnesium availability in early postnatal mice.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence-system
- Villin1-Cre conditional deletion and mineral phenotyping
- experimental_model
- Villin1-Cre conditional deletion and mineral phenotyping
- limitations
- Early developmental model; not a test of dietary Mg restriction.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Mouse
- plain_language
- Suckling mice required intestinal TRPM7 to maintain their magnesium supply.
- primary_references
- [mittermeier-2019-trpm7] TRPM7 is the central gatekeeper of intestinal mineral absorption essential for postnatal survival (2019). https://pubmed.ncbi.nlm.nih.gov/30770447/ DOI: 10.1073/pnas.1810633116
- tissue
- Intestinal enterocytes; serum
- tissue_or_cell_type
- Intestinal enterocytes; serum
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 975–986
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Villin1-Cre conditional deletion and mineral phenotyping · source_derived_draft · unverified_draft
### intestinal-trpm7-loss-magnesium Intestinal Trpm7 deletion lowered magnesium availability in early postnatal mice. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Suckling mice required intestinal TRPM7 to maintain their magnesium supply. organism: Mouse tissue_or_cell_type: Intestinal enterocytes; serum experimental_model: Villin1-Cre conditional deletion and mineral phenotyping limitations: Early developmental model; not a test of dietary Mg restriction. evidence-system: Villin1-Cre conditional deletion and mineral phenotyping tissue: Intestinal enterocytes; serum [mittermeier-2019-trpm7] TRPM7 is the central gatekeeper of intestinal mineral absorption essential for postnatal survival (2019). https://pubmed.ncbi.nlm.nih.gov/30770447/ DOI: 10.1073/pnas.1810633116
Complete structured claim and evidenceIntestinal Trpm7 deletion reduced circulating zinc in early postnatal mice.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- Shared intestinal TRPM7 machinery links zinc and magnesium availability; Mg deficiency as the cause of Zn deficiency was not demonstrated.
- evidence-system
- Conditional intestinal knockout and mineral phenotyping
- experimental_model
- Conditional intestinal knockout and mineral phenotyping
- limitations
- Not evidence that magnesium supplementation universally increases zinc absorption.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Mouse
- plain_language
- A single epithelial machinery defect depleted zinc along with magnesium.
- primary_references
- [mittermeier-2019-trpm7] TRPM7 is the central gatekeeper of intestinal mineral absorption essential for postnatal survival (2019). https://pubmed.ncbi.nlm.nih.gov/30770447/ DOI: 10.1073/pnas.1810633116
- tissue
- Intestine; serum
- tissue_or_cell_type
- Intestine; serum
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1002–1014
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Conditional intestinal knockout and mineral phenotyping · source_derived_draft · unverified_draft
### intestinal-trpm7-loss-zinc Intestinal Trpm7 deletion reduced circulating zinc in early postnatal mice. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A single epithelial machinery defect depleted zinc along with magnesium. organism: Mouse tissue_or_cell_type: Intestine; serum experimental_model: Conditional intestinal knockout and mineral phenotyping limitations: Not evidence that magnesium supplementation universally increases zinc absorption. cross_nutrient: Shared intestinal TRPM7 machinery links zinc and magnesium availability; Mg deficiency as the cause of Zn deficiency was not demonstrated. evidence-system: Conditional intestinal knockout and mineral phenotyping tissue: Intestine; serum [mittermeier-2019-trpm7] TRPM7 is the central gatekeeper of intestinal mineral absorption essential for postnatal survival (2019). https://pubmed.ncbi.nlm.nih.gov/30770447/ DOI: 10.1073/pnas.1810633116
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.