E-cadherin / CDH1: molecular mechanisms & dependencies

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.

Human evidence only

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.

Recorded relationships

Where it participates (unsigned role)

Calcium binding protected the recombinant mouse E-cadherin ectodomain from tryptic cleavage; calcium depletion caused a reversible conformational change.
Calcium ion → E-cadherin ectodomain proteolysis source_derived_draftungraded
Experimental context and source evidence
compartment_description
Extracellular domain
experimental_model
Calcium titration, electron microscopy and trypsin assay
limitations
In-vitro calcium removal is not dietary calcium deficiency; the soluble fragment did not self-associate under these assay conditions.
nutrient_topic
Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
organism
Mus musculus protein expressed in insect cells
plain_language
Bound calcium helps keep the adhesion protein folded and resistant to protease attack.
primary_references
[pokutta1994] Conformational changes of the recombinant extracellular domain of E-cadherin upon calcium binding (1994). https://febs.onlinelibrary.wiley.com/doi/10.1111/j.1432-1033.1994.tb19080.x DOI: 10.1111/j.1432-1033.1994.tb19080.x
tissue_or_cell_type
Purified extracellular domain
Calcium: mechanism-first literature curation (2026-09-17) · lines 1140–1150
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Calcium titration, electron microscopy and trypsin assay · source_derived_draft · unverified_draft
### calcium-protects-e-cadherin-from-proteolysis Calcium binding protected the recombinant mouse E-cadherin ectodomain from tryptic cleavage; calcium depletion caused a reversible conformational change. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Bound calcium helps keep the adhesion protein folded and resistant to protease attack. organism: Mus musculus protein expressed in insect cells tissue_or_cell_type: Purified extracellular domain experimental_model: Calcium titration, electron microscopy and trypsin assay limitations: In-vitro calcium removal is not dietary calcium deficiency; the soluble fragment did not self-associate under these assay conditions. compartment_description: Extracellular domain [pokutta1994] Conformational changes of the recombinant extracellular domain of E-cadherin upon calcium binding (1994). https://febs.onlinelibrary.wiley.com/doi/10.1111/j.1432-1033.1994.tb19080.x DOI: 10.1111/j.1432-1033.1994.tb19080.x
Complete structured claim and evidence
Three Ca2+ ions coordinated at the interface of mouse E-cadherin extracellular domains 1 and 2 support their extended, rigid arrangement.
Calcium ion → E-cadherin ectodomain rigidity source_derived_draftungraded
Experimental context and source evidence
compartment_description
Extracellular domain
experimental_model
Two-domain crystal structure
limitations
The crystallized fragment is not a complete living adherens junction; crystal dimer geometry alone does not define every adhesion contact.
nutrient_topic
Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
organism
Mus musculus protein
plain_language
Calcium braces the outside portion of a cell-adhesion protein.
primary_references
[nagar1996] Structural basis of calcium-induced E-cadherin rigidification and dimerization (1996). https://pubmed.ncbi.nlm.nih.gov/8598933/ DOI: 10.1038/380360a0
tissue_or_cell_type
Purified E-cadherin ectodomain
Calcium: mechanism-first literature curation (2026-09-17) · lines 1128–1138
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Two-domain crystal structure · source_derived_draft · unverified_draft
### calcium-rigidifies-e-cadherin Three Ca2+ ions coordinated at the interface of mouse E-cadherin extracellular domains 1 and 2 support their extended, rigid arrangement. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Calcium braces the outside portion of a cell-adhesion protein. organism: Mus musculus protein tissue_or_cell_type: Purified E-cadherin ectodomain experimental_model: Two-domain crystal structure limitations: The crystallized fragment is not a complete living adherens junction; crystal dimer geometry alone does not define every adhesion contact. compartment_description: Extracellular domain [nagar1996] Structural basis of calcium-induced E-cadherin rigidification and dimerization (1996). https://pubmed.ncbi.nlm.nih.gov/8598933/ DOI: 10.1038/380360a0
Complete structured claim and evidence
Dihydrocapsaicin significantly and dose-dependently inhibited the migration and invasion of gastric cancer cells NCI-N87 and HGC-27, significantly increased the expression of TRPV1 and E-cadherin proteins and inhibited the expression of N-cadherin, vimentin and Snail proteins, and functional rescue experiments confirmed that when TRPV1 expression was inhibited the inhibitory effect on migration and invasion was significantly weakened.
Dihydrocapsaicin → Migration and invasion of gastric cancer cells source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
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experimental_model
Human gastric cancer cell lines NCI-N87 and HGC-27 with western blotting and TRPV1 knockdown rescue experiments
exposure
Dihydrocapsaicin at a range of concentrations, with TRPV1 expression interfered as the test of mediation
limitations
The knockdown rescue is the strength here. Note the unusual direction: the compound raised expression of its own receptor rather than merely activating it.
nutrient_topic
Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. · Dihydrocapsaicin
organism
Human cells
plain_language
It holds gastric cancer cells in place by pushing them back towards a settled, non-migrating state.
primary_references
[dhc-p42509404] Dihydrocapsaicin suppresses the migration and invasion of gastric cancer cells by upregulating TRPV1 expression. (2026). https://pubmed.ncbi.nlm.nih.gov/42509404/ DOI: 10.1007/s11626-026-01226-3
tissue_or_cell_type
Gastric cancer cells
trigger_kind
machinery_impairment Imported condition classification; unverified.
Dihydrocapsaicin: the second capsaicinoid, the hypothermia it is used to induce, what the gut and liver do to it, and what it does without TRPV1 (2026-09-21) · lines 725–736
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human gastric cancer cell lines NCI-N87 and HGC-27 with western blotting and TRPV1 knockdown rescue experiments · source_derived_draft · unverified_draft
### dhc-gastric-cancer-migration Dihydrocapsaicin significantly and dose-dependently inhibited the migration and invasion of gastric cancer cells NCI-N87 and HGC-27, significantly increased the expression of TRPV1 and E-cadherin proteins and inhibited the expression of N-cadherin, vimentin and Snail proteins, and functional rescue experiments confirmed that when TRPV1 expression was inhibited the inhibitory effect on migration and invasion was significantly weakened. Condition category: machinery_impairment nutrient_topic: Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. plain_language: It holds gastric cancer cells in place by pushing them back towards a settled, non-migrating state. organism: Human cells tissue_or_cell_type: Gastric cancer cells experimental_model: Human gastric cancer cell lines NCI-N87 and HGC-27 with western blotting and TRPV1 knockdown rescue experiments limitations: The knockdown rescue is the strength here. Note the unusual direction: the compound raised expression of its own receptor rather than merely activating it. exposure: Dihydrocapsaicin at a range of concentrations, with TRPV1 expression interfered as the test of mediation evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/42509404.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "55ec938b5e2c0b1421c473c60c3468ad24770198ee9d1f6549c62af579bf4c4c", "start_char": 0, "end_char": 1925, "text_sha256": "55ec938b5e2c0b1421c473c60c3468ad24770198ee9d1f6549c62af579bf4c4c"} [dhc-p42509404] Dihydrocapsaicin suppresses the migration and invasion of gastric cancer cells by upregulating TRPV1 expression. (2026). https://pubmed.ncbi.nlm.nih.gov/42509404/ DOI: 10.1007/s11626-026-01226-3
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.

E-cadherin / CDH1