Component
Proline-induced mouse embryonic-stem-cell state transition
Context-specific entity; species, compartment and exposure are stated on each claim.
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
Proline addition drove a reversible mesenchymal-like, motile state in embryonic stem-cell culture, accompanied by changes in H3K9 and H3K36 methylation.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse embryonic stem-cell culture with proline exposure; primary abstract.
- limitations
- This is a cell-culture state transition, not evidence that proline changes adult human identity or universally activates oncogenes.
- nutrient_topic
- L-Proline collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Proline
- plain_language
- An amino-acid exposure can alter a cell-state program in a developmental model.
- primary_references
- L-Proline induces a mesenchymal-like invasive program in embryonic stem cells by remodeling H3K9 and H3K36 methylation. · 2013 · https://pubmed.ncbi.nlm.nih.gov/24319666/ · DOI 10.1016/j.stemcr.2013.09.001
L-Proline: synthesis, collagen processing, redox metabolism and cross-nutrient mechanisms (2026-09-19) · lines 390–396
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse embryonic stem-cell culture with proline exposure; primary abstract. · source_derived_draft · unverified_draft
## l-proline-stem-cell-state An amino-acid exposure can alter a cell-state program in a developmental model. Proline addition drove a reversible mesenchymal-like, motile state in embryonic stem-cell culture, accompanied by changes in H3K9 and H3K36 methylation. Model: Mouse embryonic stem-cell culture with proline exposure; primary abstract. Limitations: This is a cell-culture state transition, not evidence that proline changes adult human identity or universally activates oncogenes. Evidence access: Primary abstract L-Proline induces a mesenchymal-like invasive program in embryonic stem cells by remodeling H3K9 and H3K36 methylation. · 2013 · https://pubmed.ncbi.nlm.nih.gov/24319666/ · DOI 10.1016/j.stemcr.2013.09.001
Complete structured claim and evidenceAscorbic-acid addition or proline withdrawal reversed the reported proline-induced stem-cell state and reduced the associated H3K9/H3K36 methylation pattern.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse embryonic stem-cell model; reversible phenotype and histone-mark measurements.
- limitations
- The result does not establish a supplement ratio, a clinical methylation imbalance, or vitamin C depletion by ordinary proline intake.
- nutrient_topic
- L-Proline collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Proline
- plain_language
- Vitamin C and proline intersect in this experimental epigenetic response.
- primary_references
- L-Proline induces a mesenchymal-like invasive program in embryonic stem cells by remodeling H3K9 and H3K36 methylation. · 2013 · https://pubmed.ncbi.nlm.nih.gov/24319666/ · DOI 10.1016/j.stemcr.2013.09.001
L-Proline: synthesis, collagen processing, redox metabolism and cross-nutrient mechanisms (2026-09-19) · lines 398–404
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse embryonic stem-cell model; reversible phenotype and histone-mark measurements. · source_derived_draft · unverified_draft
## l-proline-stem-cell-vitamin-c Vitamin C and proline intersect in this experimental epigenetic response. Ascorbic-acid addition or proline withdrawal reversed the reported proline-induced stem-cell state and reduced the associated H3K9/H3K36 methylation pattern. Model: Mouse embryonic stem-cell model; reversible phenotype and histone-mark measurements. Limitations: The result does not establish a supplement ratio, a clinical methylation imbalance, or vitamin C depletion by ordinary proline intake. Evidence access: Primary abstract L-Proline induces a mesenchymal-like invasive program in embryonic stem cells by remodeling H3K9 and H3K36 methylation. · 2013 · https://pubmed.ncbi.nlm.nih.gov/24319666/ · DOI 10.1016/j.stemcr.2013.09.001
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.