Component
Mitochondrial NADP(H) content
Measured combined oxidized and reduced phosphorylated nicotinamide dinucleotide pool; not NAD(H).
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.
What acts on it
CRISPR deletion of NADK2 in human DLD1 cells reduced mitochondrial NADP(H) by more than 80% while whole-cell NADP(H) was not similarly depleted.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary full text
- experimental_model
- Human DLD1 cells; immunopurified mitochondrial fractions and enzyme-cycling assays.
- limitations
- A compartment-specific genetic manipulation is not equivalent to dietary niacin deficiency.
- nutrient_topic
- L-Proline collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Proline
- plain_language
- The cofactor pool inside mitochondria can fail even when a whole-cell measurement looks adequate.
- 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 54–60
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human DLD1 cells; immunopurified mitochondrial fractions and enzyme-cycling assays. · source_derived_draft · unverified_draft
## l-proline-nadk2-pool The cofactor pool inside mitochondria can fail even when a whole-cell measurement looks adequate. CRISPR deletion of NADK2 in human DLD1 cells reduced mitochondrial NADP(H) by more than 80% while whole-cell NADP(H) was not similarly depleted. Model: Human DLD1 cells; immunopurified mitochondrial fractions and enzyme-cycling assays. Limitations: A compartment-specific genetic manipulation is not equivalent to dietary niacin deficiency. 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 evidencePatient fibroblasts bearing a pathogenic NADK2 alteration had reduced mitochondrial NADP(H).
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/niacin-redox-sources/nadk2-patient-2014.abstract.txt", "locator": "Indexed abstract, genetic and fibroblast results", "start_char": 357, "end_char": 1462, "file_sha256": "0e8ce719f0454f41ce98a5c35f75c88a21f5219f0d9b574cf8a793697f39db5a", "text_sha256": "e468b1beee1be208d337cdf94488aca05296b2dd3fcbba587ca323b8db6d2c96"}
- experimental_model
- Patient-derived fibroblasts
- exposure
- Inherited NADK2 alteration
- limitations
- Single described patient context; mitochondrial NADP(H) shortage arose from kinase machinery impairment, not demonstrated dietary niacin shortage.
- nutrient_topic
- Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
- organism
- Homo sapiens
- plain_language
- The genetic defect impaired the mitochondrial phosphorylated cofactor pool.
- primary_references
- [nadk2-patient-2014] Mitochondrial NADP(H) deficiency due to a mutation in NADK2 causes dienoyl-CoA reductase deficiency with hyperlysinemia. (2014). https://pubmed.ncbi.nlm.nih.gov/24847004/ DOI: 10.1093/hmg/ddu218
- tissue_or_cell_type
- Fibroblasts
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 964–975
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Patient-derived fibroblasts · source_derived_draft · unverified_draft
### b3-redox-nadk2-patient-pool Patient fibroblasts bearing a pathogenic NADK2 alteration had reduced mitochondrial NADP(H). Condition category: machinery_impairment nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The genetic defect impaired the mitochondrial phosphorylated cofactor pool. organism: Homo sapiens tissue_or_cell_type: Fibroblasts experimental_model: Patient-derived fibroblasts limitations: Single described patient context; mitochondrial NADP(H) shortage arose from kinase machinery impairment, not demonstrated dietary niacin shortage. exposure: Inherited NADK2 alteration evidence_span: {"source_cache": "artifacts/niacin-redox-sources/nadk2-patient-2014.abstract.txt", "locator": "Indexed abstract, genetic and fibroblast results", "start_char": 357, "end_char": 1462, "file_sha256": "0e8ce719f0454f41ce98a5c35f75c88a21f5219f0d9b574cf8a793697f39db5a", "text_sha256": "e468b1beee1be208d337cdf94488aca05296b2dd3fcbba587ca323b8db6d2c96"} [nadk2-patient-2014] Mitochondrial NADP(H) deficiency due to a mutation in NADK2 causes dienoyl-CoA reductase deficiency with hyperlysinemia. (2014). https://pubmed.ncbi.nlm.nih.gov/24847004/ DOI: 10.1093/hmg/ddu218
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.