Component

Aspartate incorporation into mouse-cell nucleic acids

Context-specific entity; species, compartment and exposure are stated on each claim.

1 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.

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.

Recorded relationships

What acts on it

  1. S6K1 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

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards