Component
Uridine
Uridine. Experimental scope belongs to each linked 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.
Where it participates (unsigned role)
Galactose plus uridine improved patient 2’s transferrin isoform pattern within 14 days.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- D-Galactose (coadministered_substrate); Uridine (coadministered_substrate); Human ZIP8 (SLC39A8) (affected_protein)
- evidence_span
- {"source_cache": "artifacts/manganese-clinical-sources/riley2017.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "31e4e33ec5601d443fb2d469b2e2c7d1fd89c611db0f41938b43007952d0f005", "start_char": 0, "end_char": 1732, "text_sha256": "31e4e33ec5601d443fb2d469b2e2c7d1fd89c611db0f41938b43007952d0f005", "text_characters": 1732}
- experimental_model
- Two sisters with homozygous SLC39A8 p.Cys113Ser
- exposure
- Respiratory-chain tests in patient 1; manganese and transferrin measurements and galactose-plus-uridine response in patient 2.
- limitations
- Measurements were not performed in both sisters interchangeably. The proposed SOD2 explanation was not directly demonstrated; manganese had only recently been added and cannot explain the already observed 14-day galactose/uridine response.
- nutrient_topic
- Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
- organism
- Homo sapiens
- plain_language
- A combined substrate-support treatment improved the measured sugar pattern.
- primary_references
- [mn-clin-riley2017] A SLC39A8 variant causes manganese deficiency, and glycosylation and mitochondrial disorders. (2017). https://pubmed.ncbi.nlm.nih.gov/27995398/ DOI: 10.1007/s10545-016-0010-6
- tissue_or_cell_type
- Patient-specific liver, muscle and blood measurements
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 1230–1242
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Two sisters with homozygous SLC39A8 p.Cys113Ser · source_derived_draft · unverified_draft
### mn-clin-zip8-gal-uridine Galactose plus uridine improved patient 2’s transferrin isoform pattern within 14 days. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: A combined substrate-support treatment improved the measured sugar pattern. organism: Homo sapiens tissue_or_cell_type: Patient-specific liver, muscle and blood measurements experimental_model: Two sisters with homozygous SLC39A8 p.Cys113Ser limitations: Measurements were not performed in both sisters interchangeably. The proposed SOD2 explanation was not directly demonstrated; manganese had only recently been added and cannot explain the already observed 14-day galactose/uridine response. exposure: Respiratory-chain tests in patient 1; manganese and transferrin measurements and galactose-plus-uridine response in patient 2. cross_nutrient: D-Galactose (coadministered_substrate); Uridine (coadministered_substrate); Human ZIP8 (SLC39A8) (affected_protein) evidence_span: {"source_cache": "artifacts/manganese-clinical-sources/riley2017.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "31e4e33ec5601d443fb2d469b2e2c7d1fd89c611db0f41938b43007952d0f005", "start_char": 0, "end_char": 1732, "text_sha256": "31e4e33ec5601d443fb2d469b2e2c7d1fd89c611db0f41938b43007952d0f005", "text_characters": 1732} [mn-clin-riley2017] A SLC39A8 variant causes manganese deficiency, and glycosylation and mitochondrial disorders. (2017). https://pubmed.ncbi.nlm.nih.gov/27995398/ DOI: 10.1007/s10545-016-0010-6
Complete structured claim and evidenceS6K1 depletion blocked insulin-stimulated aspartate-carbon incorporation into RNA and DNA while sparing incorporation of supplied pyrimidines in the compared assays.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary full text
- experimental_model
- Mouse wild-type embryonic fibroblasts; S6K1 siRNA, 15-hour serum starvation, 100 nM insulin for six hours during RNA/DNA labeling, with pyrimidine salvage controls.
- limitations
- An isotope-incorporation endpoint is not a measurement of dietary aspartate efficacy.
- nutrient_topic
- L-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Aspartate
- plain_language
- Blocking new nucleotide production differs from blocking every route for supplying nucleotides.
- primary_references
- Stimulation of de novo pyrimidine synthesis by growth signaling through mTOR and S6K1. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23429703/ · DOI 10.1126/science.1228792
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
L-Aspartate: redox transfer, nitrogen partitioning 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 · Mouse wild-type embryonic fibroblasts; S6K1 siRNA, 15-hour serum starvation, 100 nM insulin for six hours during RNA/DNA labeling, with pyrimidine salvage controls. · source_derived_draft · unverified_draft
## l-aspartate-cad-s6k1-flux Blocking new nucleotide production differs from blocking every route for supplying nucleotides. S6K1 depletion blocked insulin-stimulated aspartate-carbon incorporation into RNA and DNA while sparing incorporation of supplied pyrimidines in the compared assays. Model: Mouse wild-type embryonic fibroblasts; S6K1 siRNA, 15-hour serum starvation, 100 nM insulin for six hours during RNA/DNA labeling, with pyrimidine salvage controls. Limitations: An isotope-incorporation endpoint is not a measurement of dietary aspartate efficacy. Evidence access: Primary full text Stimulation of de novo pyrimidine synthesis by growth signaling through mTOR and S6K1. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23429703/ · DOI 10.1126/science.1228792
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.