Component
Oxidative-stress readouts in NADK2-deleted human cells
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
Under the tested culture conditions, NADK2 deletion did not increase measured mitochondrial oxidative stress or disrupt mitochondrial folate pathway activity despite reduced proline synthesis.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary full text
- experimental_model
- Human cell models; ROS probes, targeted redox sensors and serine isotope tracing.
- limitations
- The authors do not exclude effects during other physiological stresses; this is not a universal claim that mitochondrial NADPH is irrelevant to antioxidant defense.
- nutrient_topic
- L-Proline collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Proline
- plain_language
- Losing this cofactor pool did not shut down every pathway that might be connected to it.
- 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 86–92
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human cell models; ROS probes, targeted redox sensors and serine isotope tracing. · source_derived_draft · unverified_draft
## l-proline-nadk2-redox-boundary Losing this cofactor pool did not shut down every pathway that might be connected to it. Under the tested culture conditions, NADK2 deletion did not increase measured mitochondrial oxidative stress or disrupt mitochondrial folate pathway activity despite reduced proline synthesis. Model: Human cell models; ROS probes, targeted redox sensors and serine isotope tracing. Limitations: The authors do not exclude effects during other physiological stresses; this is not a universal claim that mitochondrial NADPH is irrelevant to antioxidant defense. 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.