Component
LC3-II abundance in human Caco-2 cells
Measured lipidated LC3 marker; exact paralog not resolved here. Increased abundance alone is not a complete autophagic-flux assay.
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
Indicaxanthin treatment increased the LC3-II marker in Caco-2 cells.
Experimental context and source evidence
- dose
- Indicaxanthin 10, 50 and 100 micromolar
- duration
- 48 h
- evidence_access
- Primary open full text, relevant results/methods and PubMed metadata.
- evidence_scope
- literature_reviewed; model-specific source-derived curation
- experimental_model
- Human Caco-2 colorectal cancer cells
- limitations
- Marker abundance and acidic organelles are not sufficient alone to quantify complete autophagic flux. Predicted BCL2 binding remains computational; methylation associations do not prove causation.
- nutrient_topic
- Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
- organism
- Human Caco-2 colorectal cancer cells
- plain_language
- Indicaxanthin treatment increased the LC3-II marker in Caco-2 cells.
- primary_references
- Indicaxanthin Induces Autophagy in Intestinal Epithelial Cancer Cells by Epigenetic Mechanisms Involving DNA Methylation. (2023). https://pubmed.ncbi.nlm.nih.gov/37571432/ DOI: 10.3390/nu15153495
- route
- In vitro addition
- tissue
- Autophagy markers and DNA methylome
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 415–424
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Human Caco-2 colorectal cancer cells · source_derived_draft · unverified_draft
## indicaxanthin-autophagy-lc3 Indicaxanthin treatment increased the LC3-II marker in Caco-2 cells. Model/species: Human Caco-2 colorectal cancer cells Tissue: Autophagy markers and DNA methylome Exposure: Indicaxanthin 10, 50 and 100 micromolar Route: In vitro addition Duration: 48 h Limits: Marker abundance and acidic organelles are not sufficient alone to quantify complete autophagic flux. Predicted BCL2 binding remains computational; methylation associations do not prove causation. Primary reference: Indicaxanthin Induces Autophagy in Intestinal Epithelial Cancer Cells by Epigenetic Mechanisms Involving DNA Methylation. (2023). https://pubmed.ncbi.nlm.nih.gov/37571432/ DOI: 10.3390/nu15153495 Access: Primary open full text, relevant results/methods and PubMed metadata.
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.