Component
WNT-TCF target gene expression
Transcriptional output of canonical WNT signalling through TCF.
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 acts on it
Ivermectin inhibited the expression of WNT-TCF target genes and repressed C-terminal beta-catenin phosphoforms and CYCLIN D1 in a manner sensitive to okadaic acid, indicating that protein phosphatases are involved.
Experimental context and source evidence
- duration
- Not stated here
- evidence_access
- Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
- experimental_model
- Human cancer cell lines and xenografts
- exposure
- Ivermectin, with low-concentration effects rescued by direct activation with TCF-VP16
- limitations
- In vivo inhibition was selective for TCF-dependent xenografts and absent in TCF-independent ones, which supports pathway specificity but does not establish the molecular binding partner.
- organism
- Human cancer cell lines and xenografts
- plain_language
- Ivermectin inhibited the expression of WNT-TCF target genes and repressed C-terminal beta-catenin phosphoforms and CYCLIN D1 in a manner sensitive to okadaic acid, indicating that protein phosphatases are involved.
- primary_references
- The river blindness drug Ivermectin and related macrocyclic lactones inhibit WNT-TCF pathway responses in human cancer. (2014). https://pubmed.ncbi.nlm.nih.gov/25143352/ DOI: 10.15252/emmm.201404084
- route
- In vitro and in vivo xenograft
- tissue
- Canonical WNT-TCF signalling output
Ivermectin: mechanism of action across parasite, host barrier and mammalian targets (2026-09-22) · lines 200–209
Original AI-assisted curation of sixteen primary studies resolved by PubMed title search and cross-checked against live PubMed metadata. Study-specific citations, concentrations, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft
## ivermectin-wnt-tcf-blockade Ivermectin inhibited the expression of WNT-TCF target genes and repressed C-terminal beta-catenin phosphoforms and CYCLIN D1 in a manner sensitive to okadaic acid, indicating that protein phosphatases are involved. Model/species: Human cancer cell lines and xenografts Tissue/system: Canonical WNT-TCF signalling output Exposure: Ivermectin, with low-concentration effects rescued by direct activation with TCF-VP16 Route: In vitro and in vivo xenograft Duration: Not stated here Limits: In vivo inhibition was selective for TCF-dependent xenografts and absent in TCF-independent ones, which supports pathway specificity but does not establish the molecular binding partner. Primary reference: The river blindness drug Ivermectin and related macrocyclic lactones inhibit WNT-TCF pathway responses in human cancer. (2014). https://pubmed.ncbi.nlm.nih.gov/25143352/ DOI: 10.15252/emmm.201404084 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
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.