Component
Human NADK2-null cell proliferation in minimal medium
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.
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
Adding proline restored growth of NADK2-deleted human cells in minimal medium, whereas the defect was largely absent in nutrient-rich medium.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary full text
- experimental_model
- Human NADK2-knockout cell cultures; DMEM compared with DMEM/F12 and individual amino-acid add-back.
- limitations
- Cell-culture rescue does not establish a treatment for inherited NADK2 disease.
- nutrient_topic
- L-Proline collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Proline
- plain_language
- An external supply can bypass a synthesis bottleneck in these cells.
- primary_references
- Mitochondrial NADP(H) generation is essential for proline biosynthesis. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33888598/ · DOI 10.1126/science.abd5491
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
L-Proline: synthesis, collagen processing, redox metabolism and cross-nutrient mechanisms (2026-09-19) · lines 70–76
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human NADK2-knockout cell cultures; DMEM compared with DMEM/F12 and individual amino-acid add-back. · source_derived_draft · unverified_draft
## l-proline-nadk2-rescue An external supply can bypass a synthesis bottleneck in these cells. Adding proline restored growth of NADK2-deleted human cells in minimal medium, whereas the defect was largely absent in nutrient-rich medium. Model: Human NADK2-knockout cell cultures; DMEM compared with DMEM/F12 and individual amino-acid add-back. Limitations: Cell-culture rescue does not establish a treatment for inherited NADK2 disease. Evidence access: Primary full text Mitochondrial NADP(H) generation is essential for proline biosynthesis. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33888598/ · DOI 10.1126/science.abd5491
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.