Component
Human p70 S6 kinase / RPS6KB1
Context-specific entity; species, compartment and exposure are stated on each claim.
3 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 it acts on
S6K1 directly phosphorylated CAD at Ser1859, connecting mTORC1 signaling to increased de novo pyrimidine synthesis.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Human HEK293E CAD expression, phosphosite mutation and kinase assays; complementary mouse cell tracing.
- limitations
- This is a signaling dependency, not evidence that a specific nutrient supplement necessarily increases CAD activity.
- nutrient_topic
- L-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Aspartate
- plain_language
- Growth signals can accelerate use of aspartate for nucleotide production.
- 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
L-Aspartate: redox transfer, nitrogen partitioning 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 HEK293E CAD expression, phosphosite mutation and kinase assays; complementary mouse cell tracing. · source_derived_draft · unverified_draft
## l-aspartate-cad-s6k1 Growth signals can accelerate use of aspartate for nucleotide production. S6K1 directly phosphorylated CAD at Ser1859, connecting mTORC1 signaling to increased de novo pyrimidine synthesis. Model: Human HEK293E CAD expression, phosphosite mutation and kinase assays; complementary mouse cell tracing. Limitations: This is a signaling dependency, not evidence that a specific nutrient supplement necessarily increases CAD activity. 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
What acts on it
Cell-free competition and activity assays supported fisetin binding and inhibition of p70S6K in the human melanoma study.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human melanoma models plus cell-free kinase assays.
- limitations
- Docking was supplemented by biochemical assays; clinical target engagement remains unproven.
- nutrient_topic
- Fisetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Fisetin
- plain_language
- A binding assay supports a more direct target relationship.
- primary_references
- Fisetin inhibits human melanoma cell growth through direct binding to p70S6K and mTOR: findings from 3-D melanoma skin equivalents and computational modeling. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24675012/ · DOI 10.1016/j.bcp.2014.03.007
Fisetin: metabolism, cell-state responses and cross-nutrient mechanisms (2026-09-19) · lines 280–286
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human melanoma models plus cell-free kinase assays. · source_derived_draft · unverified_draft
## fisetin-s6k-binding A binding assay supports a more direct target relationship. Cell-free competition and activity assays supported fisetin binding and inhibition of p70S6K in the human melanoma study. Model: Human melanoma models plus cell-free kinase assays. Limitations: Docking was supplemented by biochemical assays; clinical target engagement remains unproven. Evidence access: Primary abstract Fisetin inhibits human melanoma cell growth through direct binding to p70S6K and mTOR: findings from 3-D melanoma skin equivalents and computational modeling. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24675012/ · DOI 10.1016/j.bcp.2014.03.007
Complete structured claim and evidence
Where it participates (unsigned role)
Satellite cells expressing NCAM and Pax7 increased 24 to 48 hours after exercise with active recovery, and numbers were greater after active recovery than after immersion, while phosphorylation of p70S6 kinase at Thr421/Ser424 increased after exercise in both conditions but was greater after active recovery.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/cold-research/26174323.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "91eff53ecc4779637af3d6fd47a67892729e3a896fdc8738f69d1c7936b4787d", "start_char": 0, "end_char": 1595, "text_sha256": "91eff53ecc4779637af3d6fd47a67892729e3a896fdc8738f69d1c7936b4787d"}
- experimental_model
- Twelve weeks of strength training in 21 men with immersion or active recovery, plus a biopsy study in nine men
- exposure
- 10 minutes of cold water immersion after each training session, twice weekly for 12 weeks
- limitations
- A randomised training study with muscle biopsies. It measures long-term adaptation rather than acute recovery, which is why it can disagree with the soreness literature without contradicting it.
- nutrient_topic
- Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Cold water immersion
- organism
- Human
- plain_language
- The repair cells that build new muscle showed up in smaller numbers after the cold.
- primary_references
- [cold-p26174323] Post-exercise cold water immersion attenuates acute anabolic signalling and long-term adaptations in muscle to strength training. (2015). https://pubmed.ncbi.nlm.nih.gov/26174323/ DOI: 10.1113/jp270570
- tissue_or_cell_type
- Skeletal muscle
Cold water immersion: cold sensing, heat production, the catecholamine axis and what repeated exposure changes (2026-09-19) · lines 819–830
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Twelve weeks of strength training in 21 men with immersion or active recovery, plus a biopsy study in nine men · source_derived_draft · unverified_draft
### cold-cwi-satellite-cells Satellite cells expressing NCAM and Pax7 increased 24 to 48 hours after exercise with active recovery, and numbers were greater after active recovery than after immersion, while phosphorylation of p70S6 kinase at Thr421/Ser424 increased after exercise in both conditions but was greater after active recovery. Condition category: normal nutrient_topic: Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The repair cells that build new muscle showed up in smaller numbers after the cold. organism: Human tissue_or_cell_type: Skeletal muscle experimental_model: Twelve weeks of strength training in 21 men with immersion or active recovery, plus a biopsy study in nine men limitations: A randomised training study with muscle biopsies. It measures long-term adaptation rather than acute recovery, which is why it can disagree with the soreness literature without contradicting it. exposure: 10 minutes of cold water immersion after each training session, twice weekly for 12 weeks evidence_span: {"source_cache": "artifacts/cold-research/26174323.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "91eff53ecc4779637af3d6fd47a67892729e3a896fdc8738f69d1c7936b4787d", "start_char": 0, "end_char": 1595, "text_sha256": "91eff53ecc4779637af3d6fd47a67892729e3a896fdc8738f69d1c7936b4787d"} [cold-p26174323] Post-exercise cold water immersion attenuates acute anabolic signalling and long-term adaptations in muscle to strength training. (2015). https://pubmed.ncbi.nlm.nih.gov/26174323/ DOI: 10.1113/jp270570
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.