Component
Intestinal crypt endoplasmic-reticulum stress
Intestinal crypt endoplasmic-reticulum stress; model and exposure are recorded in linked claims.
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 acts on it
Intestinal epithelial Zip7 deletion increased ER-stress responses in proliferative progenitor cells and was followed by substantial progenitor-cell death.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- Mouse ZIP7 / Slc39a7 (affected_transporter); Intestinal progenitor-cell survival (reduced_endpoint)
- evidence_span
- {"source_cache": "artifacts/zinc-signaling-sources/27736879-abstract.txt", "locator": "Primary indexed abstract", "file_sha256": "4ce8fe391aff141b5145e4122917ca1c1817273ab0dd55c7a936b687d9dacdd6"}
- experimental_model
- Conditional intestinal Zip7-deficient mice and organoids
- exposure
- Intestinal epithelial versus Lgr5-cell-specific deletion; zinc supplementation comparison.
- limitations
- Cell lineage and tissue context matter. Supplementation failing to rescue a transporter defect is not evidence that ordinary dietary zinc replacement fails.
- nutrient_topic
- Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
- organism
- Mus musculus
- plain_language
- Loss of zinc distribution machinery stressed the cells that renew the intestinal lining.
- primary_references
- [zn-sig-27736879] Zinc Transporter SLC39A7/ZIP7 Promotes Intestinal Epithelial Self-Renewal by Resolving ER Stress. (2016). https://pubmed.ncbi.nlm.nih.gov/27736879/ DOI: 10.1371/journal.pgen.1006349
- tissue_or_cell_type
- Intestinal crypts, progenitor cells and organoids
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 1125–1137
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Conditional intestinal Zip7-deficient mice and organoids · source_derived_draft · unverified_draft
### zn-sig-zip7-er-stress Intestinal epithelial Zip7 deletion increased ER-stress responses in proliferative progenitor cells and was followed by substantial progenitor-cell death. Condition category: machinery_impairment nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Loss of zinc distribution machinery stressed the cells that renew the intestinal lining. organism: Mus musculus tissue_or_cell_type: Intestinal crypts, progenitor cells and organoids experimental_model: Conditional intestinal Zip7-deficient mice and organoids limitations: Cell lineage and tissue context matter. Supplementation failing to rescue a transporter defect is not evidence that ordinary dietary zinc replacement fails. exposure: Intestinal epithelial versus Lgr5-cell-specific deletion; zinc supplementation comparison. cross_nutrient: Mouse ZIP7 / Slc39a7 (affected_transporter); Intestinal progenitor-cell survival (reduced_endpoint) evidence_span: {"source_cache": "artifacts/zinc-signaling-sources/27736879-abstract.txt", "locator": "Primary indexed abstract", "file_sha256": "4ce8fe391aff141b5145e4122917ca1c1817273ab0dd55c7a936b687d9dacdd6"} [zn-sig-27736879] Zinc Transporter SLC39A7/ZIP7 Promotes Intestinal Epithelial Self-Renewal by Resolving ER Stress. (2016). https://pubmed.ncbi.nlm.nih.gov/27736879/ DOI: 10.1371/journal.pgen.1006349
Complete structured claim and evidenceAdding 1 µM ZnSO4 did not suppress ER-stress gene induction in Zip7-deficient intestinal organoids assessed 48 hours after induction of deletion; the study also observed no rescue in fibroblasts, while restored ZIP7 expression rescued their stress response.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- Mouse ZIP7 / Slc39a7 (affected_transporter)
- evidence_span
- {"source_cache": "artifacts/zinc-signaling-sources/27736879.txt", "locator": "Results: Zip7 deletion activates ER stress; Figure 4, Figure 5 and supplemental Figure S8", "file_sha256": "4771f8b4a2b4e332b10bd2a5abef6f538cc38f4c85916b44ddab9f15679ed621"}
- experimental_model
- Conditional intestinal Zip7-deficient mice and organoids
- exposure
- Supplemental Figure S8: 1 µM ZnSO4; intestinal organoids assessed 48 hours after the study-induced Zip7 deletion. The fibroblast comparison also used 1 µM ZnSO4. This exposure did not suppress the measured ER-stress gene induction.
- limitations
- Cell lineage and tissue context matter. Supplementation failing to rescue a transporter defect is not evidence that ordinary dietary zinc replacement fails.
- nutrient_topic
- Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
- organism
- Mus musculus
- plain_language
- More available zinc did not substitute for the missing distribution machinery.
- primary_references
- [zn-sig-27736879] Zinc Transporter SLC39A7/ZIP7 Promotes Intestinal Epithelial Self-Renewal by Resolving ER Stress. (2016). https://pubmed.ncbi.nlm.nih.gov/27736879/ DOI: 10.1371/journal.pgen.1006349
- tissue_or_cell_type
- Intestinal crypts, progenitor cells and organoids
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 1139–1151
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Conditional intestinal Zip7-deficient mice and organoids · source_derived_draft · unverified_draft
### zn-sig-zip7-zinc-no-rescue Adding 1 µM ZnSO4 did not suppress ER-stress gene induction in Zip7-deficient intestinal organoids assessed 48 hours after induction of deletion; the study also observed no rescue in fibroblasts, while restored ZIP7 expression rescued their stress response. Condition category: machinery_impairment nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: More available zinc did not substitute for the missing distribution machinery. organism: Mus musculus tissue_or_cell_type: Intestinal crypts, progenitor cells and organoids experimental_model: Conditional intestinal Zip7-deficient mice and organoids limitations: Cell lineage and tissue context matter. Supplementation failing to rescue a transporter defect is not evidence that ordinary dietary zinc replacement fails. exposure: Supplemental Figure S8: 1 µM ZnSO4; intestinal organoids assessed 48 hours after the study-induced Zip7 deletion. The fibroblast comparison also used 1 µM ZnSO4. This exposure did not suppress the measured ER-stress gene induction. cross_nutrient: Mouse ZIP7 / Slc39a7 (affected_transporter) evidence_span: {"source_cache": "artifacts/zinc-signaling-sources/27736879.txt", "locator": "Results: Zip7 deletion activates ER stress; Figure 4, Figure 5 and supplemental Figure S8", "file_sha256": "4771f8b4a2b4e332b10bd2a5abef6f538cc38f4c85916b44ddab9f15679ed621"} [zn-sig-27736879] Zinc Transporter SLC39A7/ZIP7 Promotes Intestinal Epithelial Self-Renewal by Resolving ER Stress. (2016). https://pubmed.ncbi.nlm.nih.gov/27736879/ DOI: 10.1371/journal.pgen.1006349
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.