Component
Human lysosome-to-cytosol polyamine export
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
ATP13A2 supports lysosomal polyamine export to cytosol after endocytic uptake; spermine had the highest tested affinity.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Purified human transporter and cellular transport experiments.
- limitations
- Polyamine-class result; strongest affinity was for spermine, not necessarily spermidine.
- nutrient_topic
- Spermidine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Spermidine
- plain_language
- A molecule can enter a cell yet remain trapped in a compartment.
- primary_references
- ATP13A2 deficiency disrupts lysosomal polyamine export. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31996848/ · DOI 10.1038/s41586-020-1968-7
Spermidine: biosynthesis, hypusination, transport and cross-nutrient mechanisms (2026-09-19) · lines 118–124
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Purified human transporter and cellular transport experiments. · source_derived_draft · unverified_draft
## spermidine-atp13a2-export A molecule can enter a cell yet remain trapped in a compartment. ATP13A2 supports lysosomal polyamine export to cytosol after endocytic uptake; spermine had the highest tested affinity. Model: Purified human transporter and cellular transport experiments. Limitations: Polyamine-class result; strongest affinity was for spermine, not necessarily spermidine. Evidence access: Primary abstract ATP13A2 deficiency disrupts lysosomal polyamine export. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31996848/ · DOI 10.1038/s41586-020-1968-7
Complete structured claim and evidenceLoss or disease-associated impairment of ATP13A2 reduced export function and worsened high-polyamine lysosomal injury.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Human transporter/cell experiments; neuronal and nematode validation in the paper.
- limitations
- Do not infer that dietary spermidine treats ATP13A2 disease; high-exposure findings retain their context.
- nutrient_topic
- Spermidine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Spermidine
- plain_language
- A transport defect can make extra polyamine harmful.
- primary_references
- ATP13A2 deficiency disrupts lysosomal polyamine export. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31996848/ · DOI 10.1038/s41586-020-1968-7
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Spermidine: biosynthesis, hypusination, transport and cross-nutrient mechanisms (2026-09-19) · lines 126–132
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human transporter/cell experiments; neuronal and nematode validation in the paper. · source_derived_draft · unverified_draft
## spermidine-atp13a2-failure A transport defect can make extra polyamine harmful. Loss or disease-associated impairment of ATP13A2 reduced export function and worsened high-polyamine lysosomal injury. Model: Human transporter/cell experiments; neuronal and nematode validation in the paper. Limitations: Do not infer that dietary spermidine treats ATP13A2 disease; high-exposure findings retain their context. Evidence access: Primary abstract ATP13A2 deficiency disrupts lysosomal polyamine export. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31996848/ · DOI 10.1038/s41586-020-1968-7
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.