Component
Human protein arginine methyltransferase 5 / PRMT5
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
MAT2A depletion preferentially reduced growth and PRMT5 methylation activity in MTAP-deleted cells.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Human cancer-cell genetic depletion experiments.
- limitations
- This genetic interaction is not proof of efficacy for methionine restriction or a particular drug in patients.
- nutrient_topic
- L-Methionine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Methionine
- plain_language
- Loss of a recycling enzyme can make cells more sensitive to reduced donor synthesis.
- primary_references
- MTAP Deletions in Cancer Create Vulnerability to Targeting of the MAT2A/PRMT5/RIOK1 Axis. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27068473/ · DOI 10.1016/j.celrep.2016.03.043
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
L-Methionine: transport, methylation, sulfur metabolism and cross-nutrient mechanisms (2026-09-19) · lines 300–306
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human cancer-cell genetic depletion experiments. · source_derived_draft · unverified_draft
## methionine-mat2a-prmt5-vulnerability Loss of a recycling enzyme can make cells more sensitive to reduced donor synthesis. MAT2A depletion preferentially reduced growth and PRMT5 methylation activity in MTAP-deleted cells. Model: Human cancer-cell genetic depletion experiments. Limitations: This genetic interaction is not proof of efficacy for methionine restriction or a particular drug in patients. Evidence access: Primary abstract MTAP Deletions in Cancer Create Vulnerability to Targeting of the MAT2A/PRMT5/RIOK1 Axis. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27068473/ · DOI 10.1016/j.celrep.2016.03.043
Complete structured claim and evidenceBiochemical methyltransferase profiling identified MTA as a potent selective PRMT5 inhibitor; MTAP-deleted cells had reduced PRMT5 methylation activity.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human cancer-cell and purified-enzyme study.
- limitations
- Selectivity applies to the tested panel and conditions; not all methyltransferases.
- nutrient_topic
- L-Methionine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Methionine
- plain_language
- A recycling product can inhibit another methylation enzyme.
- primary_references
- MTAP Deletions in Cancer Create Vulnerability to Targeting of the MAT2A/PRMT5/RIOK1 Axis. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27068473/ · DOI 10.1016/j.celrep.2016.03.043
L-Methionine: transport, methylation, sulfur metabolism and cross-nutrient mechanisms (2026-09-19) · lines 292–298
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human cancer-cell and purified-enzyme study. · source_derived_draft · unverified_draft
## methionine-mta-prmt5 A recycling product can inhibit another methylation enzyme. Biochemical methyltransferase profiling identified MTA as a potent selective PRMT5 inhibitor; MTAP-deleted cells had reduced PRMT5 methylation activity. Model: Human cancer-cell and purified-enzyme study. Limitations: Selectivity applies to the tested panel and conditions; not all methyltransferases. Evidence access: Primary abstract MTAP Deletions in Cancer Create Vulnerability to Targeting of the MAT2A/PRMT5/RIOK1 Axis. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27068473/ · DOI 10.1016/j.celrep.2016.03.043
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.