Component
Human LOX IMVI cell proliferation
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
Removing extracellular glycine alone slowed LOX IMVI proliferation but did not impair A498 cells in the same study.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- evidence_access
- Primary full text
- experimental_model
- Human cancer-cell comparison under culture glycine withdrawal.
- limitations
- A local experimental shortage, not a universal human dietary deficiency threshold.
- nutrient_topic
- Glycine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Glycine
- plain_language
- Some cells depend more on imported glycine than others.
- primary_references
- Metabolite profiling identifies a key role for glycine in rapid cancer cell proliferation. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22628656/ · DOI 10.1126/science.1218595
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Glycine: supply, one-carbon allocation, receptors and cross-nutrient mechanisms (2026-09-19) · lines 162–168
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human cancer-cell comparison under culture glycine withdrawal. · source_derived_draft · unverified_draft
## glycine-glycine-withdrawal Some cells depend more on imported glycine than others. Removing extracellular glycine alone slowed LOX IMVI proliferation but did not impair A498 cells in the same study. Model: Human cancer-cell comparison under culture glycine withdrawal. Limitations: A local experimental shortage, not a universal human dietary deficiency threshold. Evidence access: Primary full text Metabolite profiling identifies a key role for glycine in rapid cancer cell proliferation. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22628656/ · DOI 10.1126/science.1218595
Complete structured claim and evidenceSHMT2 silencing combined with removal of extracellular glycine halted LOX IMVI proliferation; adding glycine restored growth whereas formate did not.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary full text
- experimental_model
- Human melanoma cultures with shRNA and nutrient withdrawal/rescue.
- limitations
- A combined manipulation; not proof that ordinary dietary glycine alone controls a tumor.
- nutrient_topic
- Glycine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Glycine
- plain_language
- Removing both synthesis and external supply exposed a glycine dependency.
- primary_references
- Metabolite profiling identifies a key role for glycine in rapid cancer cell proliferation. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22628656/ · DOI 10.1126/science.1218595
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Glycine: supply, one-carbon allocation, receptors and cross-nutrient mechanisms (2026-09-19) · lines 154–160
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human melanoma cultures with shRNA and nutrient withdrawal/rescue. · source_derived_draft · unverified_draft
## glycine-shmt2-glycine-dependence Removing both synthesis and external supply exposed a glycine dependency. SHMT2 silencing combined with removal of extracellular glycine halted LOX IMVI proliferation; adding glycine restored growth whereas formate did not. Model: Human melanoma cultures with shRNA and nutrient withdrawal/rescue. Limitations: A combined manipulation; not proof that ordinary dietary glycine alone controls a tumor. Evidence access: Primary full text Metabolite profiling identifies a key role for glycine in rapid cancer cell proliferation. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22628656/ · DOI 10.1126/science.1218595
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.