Component

NADK2 Δ62 recombinant construct

Purified experimental human NADK2 lacking the N-terminal 62 residues; not an unqualified native isoform.

4 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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 it acts on

  1. The tested NADH kinase activity of purified human NADK2 Δ62 was about 10% of its NAD+ kinase activity.

    NADK2 Δ62 recombinant construct → NADH source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/niacin-redox-sources/nadk2-2012.fulltext.txt", "locator": "Results", "start_char": 9582, "end_char": 11594, "file_sha256": "65209c0b4ea7220bc95afdd182e40910f2445345172956e85552d5c6db649648", "text_sha256": "ffd25dd072f6f8f486b11ca632f28acf37e3ef2b0dbd2b20eecf32fce649eaf1"}
    experimental_model
    Purified NADK2 Δ62
    exposure
    ATP-dependent NADH versus NAD+ assays
    limitations
    Relative activity under the reported substrate conditions; not a universal cellular flux ratio.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Homo sapiens
    plain_language
    NADK2 could phosphorylate NADH in this assay, but favored NAD+.
    primary_references
    [nadk2-2012] Identification and characterization of a human mitochondrial NAD kinase. (2012). https://pubmed.ncbi.nlm.nih.gov/23212377/ DOI: 10.1038/ncomms2262
    tissue_or_cell_type
    Purified enzyme

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 899–910

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified NADK2 Δ62 · source_derived_draft · unverified_draft

    ### b3-redox-nadk2-nadh-preference The tested NADH kinase activity of purified human NADK2 Δ62 was about 10% of its NAD+ kinase activity. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: NADK2 could phosphorylate NADH in this assay, but favored NAD+. organism: Homo sapiens tissue_or_cell_type: Purified enzyme experimental_model: Purified NADK2 Δ62 limitations: Relative activity under the reported substrate conditions; not a universal cellular flux ratio. exposure: ATP-dependent NADH versus NAD+ assays evidence_span: {"source_cache": "artifacts/niacin-redox-sources/nadk2-2012.fulltext.txt", "locator": "Results", "start_char": 9582, "end_char": 11594, "file_sha256": "65209c0b4ea7220bc95afdd182e40910f2445345172956e85552d5c6db649648", "text_sha256": "ffd25dd072f6f8f486b11ca632f28acf37e3ef2b0dbd2b20eecf32fce649eaf1"} [nadk2-2012] Identification and characterization of a human mitochondrial NAD kinase. (2012). https://pubmed.ncbi.nlm.nih.gov/23212377/ DOI: 10.1038/ncomms2262
    Complete structured claim and evidence

  2. Purified human NADK2 Δ62 converted NAD+ to NADP+ with ATP in MgCl2-containing reactions; TLC also detected ADP formation.

    NADK2 Δ62 recombinant construct → NADP+ source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Magnesium is present with ATP during phosphorylation of the niacin-derived dinucleotide; this assay does not quantify effects of dietary magnesium shortage.
    evidence_span
    [{"source_cache": "artifacts/niacin-redox-sources/nadk2-2012.fulltext.txt", "locator": "Results", "start_char": 8475, "end_char": 9580, "file_sha256": "65209c0b4ea7220bc95afdd182e40910f2445345172956e85552d5c6db649648", "text_sha256": "c86810a1a5342cd4e7ea126e070f28ed3182d81f17ea76c0fbb3833612c0f529"}, {"source_cache": "artifacts/niacin-redox-sources/nadk2-2012.fulltext.txt", "locator": "Methods, NADK activity assay", "start_char": 26694, "end_char": 28732, "file_sha256": "65209c0b4ea7220bc95afdd182e40910f2445345172956e85552d5c6db649648", "text_sha256": "907b651f0c0aae7a31306bdc42264cdfd22fb0e236e7ab8f37900467b0b0ab72"}]
    experimental_model
    Purified His-tagged Δ62C5orf33/NADK2
    exposure
    TLC: 5 mM NAD+, 5 mM ATP, 5 mM MgCl2; 37°C
    limitations
    Scoped experimental observation; no dietary niacin or magnesium deficiency threshold or treatment benefit was tested.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Homo sapiens
    plain_language
    The mitochondrial kinase uses a phosphate-transfer reaction to create NADP+.
    primary_references
    [nadk2-2012] Identification and characterization of a human mitochondrial NAD kinase. (2012). https://pubmed.ncbi.nlm.nih.gov/23212377/ DOI: 10.1038/ncomms2262
    tissue_or_cell_type
    Purified protein

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 871–883

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified His-tagged Δ62C5orf33/NADK2 · source_derived_draft · unverified_draft

    ### b3-redox-nadk2-phosphorylation Purified human NADK2 Δ62 converted NAD+ to NADP+ with ATP in MgCl2-containing reactions; TLC also detected ADP formation. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The mitochondrial kinase uses a phosphate-transfer reaction to create NADP+. organism: Homo sapiens tissue_or_cell_type: Purified protein experimental_model: Purified His-tagged Δ62C5orf33/NADK2 limitations: Scoped experimental observation; no dietary niacin or magnesium deficiency threshold or treatment benefit was tested. exposure: TLC: 5 mM NAD+, 5 mM ATP, 5 mM MgCl2; 37°C cross_nutrient: Magnesium is present with ATP during phosphorylation of the niacin-derived dinucleotide; this assay does not quantify effects of dietary magnesium shortage. evidence_span: [{"source_cache": "artifacts/niacin-redox-sources/nadk2-2012.fulltext.txt", "locator": "Results", "start_char": 8475, "end_char": 9580, "file_sha256": "65209c0b4ea7220bc95afdd182e40910f2445345172956e85552d5c6db649648", "text_sha256": "c86810a1a5342cd4e7ea126e070f28ed3182d81f17ea76c0fbb3833612c0f529"}, {"source_cache": "artifacts/niacin-redox-sources/nadk2-2012.fulltext.txt", "locator": "Methods, NADK activity assay", "start_char": 26694, "end_char": 28732, "file_sha256": "65209c0b4ea7220bc95afdd182e40910f2445345172956e85552d5c6db649648", "text_sha256": "907b651f0c0aae7a31306bdc42264cdfd22fb0e236e7ab8f37900467b0b0ab72"}] [nadk2-2012] Identification and characterization of a human mitochondrial NAD kinase. (2012). https://pubmed.ncbi.nlm.nih.gov/23212377/ DOI: 10.1038/ncomms2262
    Complete structured claim and evidence

  3. Purified human NADK2 Δ62 also supported NADP+ formation using inorganic polyphosphate preparations as phosphate donors.

    NADK2 Δ62 recombinant construct → Inorganic polyphosphate source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Uses phosphate polymers in a magnesium-containing enzyme assay, not a dietary phosphorus intervention.
    evidence_span
    {"source_cache": "artifacts/niacin-redox-sources/nadk2-2012.fulltext.txt", "locator": "Results", "start_char": 11596, "end_char": 12294, "file_sha256": "65209c0b4ea7220bc95afdd182e40910f2445345172956e85552d5c6db649648", "text_sha256": "f371b72f3f7104e6b2b1f4f28ec55e04b18b931383b51a3258872db0809a10d9"}
    experimental_model
    Purified NADK2 Δ62
    exposure
    Metaphosphate, hexametaphosphate and tetrapolyphosphate tested
    limitations
    In vitro substrate capacity; physiological flux from polyphosphate in human mitochondria was not established. Monomeric phosphate is not interchangeable with these polymers.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Homo sapiens
    plain_language
    The recombinant mitochondrial enzyme accepted some polyphosphate preparations in vitro.
    primary_references
    [nadk2-2012] Identification and characterization of a human mitochondrial NAD kinase. (2012). https://pubmed.ncbi.nlm.nih.gov/23212377/ DOI: 10.1038/ncomms2262
    tissue_or_cell_type
    Purified enzyme

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 885–897

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified NADK2 Δ62 · source_derived_draft · unverified_draft

    ### b3-redox-nadk2-polyphosphate Purified human NADK2 Δ62 also supported NADP+ formation using inorganic polyphosphate preparations as phosphate donors. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The recombinant mitochondrial enzyme accepted some polyphosphate preparations in vitro. organism: Homo sapiens tissue_or_cell_type: Purified enzyme experimental_model: Purified NADK2 Δ62 limitations: In vitro substrate capacity; physiological flux from polyphosphate in human mitochondria was not established. Monomeric phosphate is not interchangeable with these polymers. exposure: Metaphosphate, hexametaphosphate and tetrapolyphosphate tested cross_nutrient: Uses phosphate polymers in a magnesium-containing enzyme assay, not a dietary phosphorus intervention. evidence_span: {"source_cache": "artifacts/niacin-redox-sources/nadk2-2012.fulltext.txt", "locator": "Results", "start_char": 11596, "end_char": 12294, "file_sha256": "65209c0b4ea7220bc95afdd182e40910f2445345172956e85552d5c6db649648", "text_sha256": "f371b72f3f7104e6b2b1f4f28ec55e04b18b931383b51a3258872db0809a10d9"} [nadk2-2012] Identification and characterization of a human mitochondrial NAD kinase. (2012). https://pubmed.ncbi.nlm.nih.gov/23212377/ DOI: 10.1038/ncomms2262
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Full-length human NADK2 localized to mitochondria in HEK293A cells; deletion of its first 62 residues disrupted that localization.

    NADK2 → Mitochondria source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/niacin-redox-sources/nadk2-2012.fulltext.txt", "locator": "Results", "start_char": 12522, "end_char": 13722, "file_sha256": "65209c0b4ea7220bc95afdd182e40910f2445345172956e85552d5c6db649648", "text_sha256": "bdd61af93db3bf8e573fc599daf7a38da7f5b844d9b5da00d86e955657611875"}
    experimental_model
    FLAG-tagged proteins and endogenous-protein fractionation
    exposure
    Full-length versus Δ62 construct
    limitations
    Evidence resolves mitochondrial localization, not precise submitochondrial position.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Homo sapiens
    plain_language
    The N-terminal targeting region directs this kinase into mitochondria.
    primary_references
    [nadk2-2012] Identification and characterization of a human mitochondrial NAD kinase. (2012). https://pubmed.ncbi.nlm.nih.gov/23212377/ DOI: 10.1038/ncomms2262
    tissue_or_cell_type
    HEK293A cells

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 912–923

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · FLAG-tagged proteins and endogenous-protein fractionation · source_derived_draft · unverified_draft

    ### b3-redox-nadk2-localization Full-length human NADK2 localized to mitochondria in HEK293A cells; deletion of its first 62 residues disrupted that localization. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The N-terminal targeting region directs this kinase into mitochondria. organism: Homo sapiens tissue_or_cell_type: HEK293A cells experimental_model: FLAG-tagged proteins and endogenous-protein fractionation limitations: Evidence resolves mitochondrial localization, not precise submitochondrial position. exposure: Full-length versus Δ62 construct evidence_span: {"source_cache": "artifacts/niacin-redox-sources/nadk2-2012.fulltext.txt", "locator": "Results", "start_char": 12522, "end_char": 13722, "file_sha256": "65209c0b4ea7220bc95afdd182e40910f2445345172956e85552d5c6db649648", "text_sha256": "bdd61af93db3bf8e573fc599daf7a38da7f5b844d9b5da00d86e955657611875"} [nadk2-2012] Identification and characterization of a human mitochondrial NAD kinase. (2012). https://pubmed.ncbi.nlm.nih.gov/23212377/ DOI: 10.1038/ncomms2262
    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