Component

Human CD38

Human CD38 NAD glycohydrolase/ADP-ribosyl cyclase.

6 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. Human CD38 also hydrolyzes cyclic ADP-ribose to ADP-ribose.

    Human CD38 → Cyclic ADP-ribose source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    evidence_span
    {"source_cache": "artifacts/niacin-consumption-sources/cd381998.abstract.txt", "locator": "Indexed abstract", "start_char": 0, "end_char": 1755, "file_sha256": "39f90bb382ddfee34e808fc93c5a1afafc1d9638a9dc73f2770e815827b4f2ad", "text_sha256": "39f90bb382ddfee34e808fc93c5a1afafc1d9638a9dc73f2770e815827b4f2ad"}
    experimental_model
    Biochemical characterization of human CD38
    exposure
    Cyclic ADP-ribose substrate
    limitations
    Primary human enzyme study; source abstract used. Product proportions are assay-specific and do not establish tissue flux or supplementation outcomes.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Human
    plain_language
    CD38 also breaks down cyclic ADP-ribose.
    primary_references
    [b3-cons-cd381998] Human CD38 is an authentic NAD(P)+ glycohydrolase. (1998). https://pubmed.ncbi.nlm.nih.gov/9494110/ DOI: 10.1042/bj3301383
    tissue_or_cell_type
    Cell-free enzyme preparation

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 593–605

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Biochemical characterization of human CD38 · source_derived_draft · unverified_draft

    ### b3-cons-cd38-cadpr-hydrolysis Human CD38 also hydrolyzes cyclic ADP-ribose to ADP-ribose. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: CD38 also breaks down cyclic ADP-ribose. organism: Human tissue_or_cell_type: Cell-free enzyme preparation experimental_model: Biochemical characterization of human CD38 limitations: Primary human enzyme study; source abstract used. Product proportions are assay-specific and do not establish tissue flux or supplementation outcomes. exposure: Cyclic ADP-ribose substrate cross_nutrient: false evidence_span: {"source_cache": "artifacts/niacin-consumption-sources/cd381998.abstract.txt", "locator": "Indexed abstract", "start_char": 0, "end_char": 1755, "file_sha256": "39f90bb382ddfee34e808fc93c5a1afafc1d9638a9dc73f2770e815827b4f2ad", "text_sha256": "39f90bb382ddfee34e808fc93c5a1afafc1d9638a9dc73f2770e815827b4f2ad"} [b3-cons-cd381998] Human CD38 is an authentic NAD(P)+ glycohydrolase. (1998). https://pubmed.ncbi.nlm.nih.gov/9494110/ DOI: 10.1042/bj3301383
    Complete structured claim and evidence

  2. Human CD38 produces cyclic ADP-ribose as a low-efficiency branch of NAD+ cleavage.

    Human CD38 → Cyclic ADP-ribose source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    evidence_span
    {"source_cache": "artifacts/niacin-consumption-sources/cd381998.abstract.txt", "locator": "Indexed abstract", "start_char": 0, "end_char": 1755, "file_sha256": "39f90bb382ddfee34e808fc93c5a1afafc1d9638a9dc73f2770e815827b4f2ad", "text_sha256": "39f90bb382ddfee34e808fc93c5a1afafc1d9638a9dc73f2770e815827b4f2ad"}
    experimental_model
    Biochemical characterization of human CD38
    exposure
    NAD+ as substrate
    limitations
    Primary human enzyme study; source abstract used. Product proportions are assay-specific and do not establish tissue flux or supplementation outcomes.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Human
    plain_language
    Some CD38 cleavage produces the cyclic calcium messenger.
    primary_references
    [b3-cons-cd381998] Human CD38 is an authentic NAD(P)+ glycohydrolase. (1998). https://pubmed.ncbi.nlm.nih.gov/9494110/ DOI: 10.1042/bj3301383
    tissue_or_cell_type
    Cell-free enzyme preparation

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 579–591

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Biochemical characterization of human CD38 · source_derived_draft · unverified_draft

    ### b3-cons-cd38-cyclization Human CD38 produces cyclic ADP-ribose as a low-efficiency branch of NAD+ cleavage. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Some CD38 cleavage produces the cyclic calcium messenger. organism: Human tissue_or_cell_type: Cell-free enzyme preparation experimental_model: Biochemical characterization of human CD38 limitations: Primary human enzyme study; source abstract used. Product proportions are assay-specific and do not establish tissue flux or supplementation outcomes. exposure: NAD+ as substrate cross_nutrient: false evidence_span: {"source_cache": "artifacts/niacin-consumption-sources/cd381998.abstract.txt", "locator": "Indexed abstract", "start_char": 0, "end_char": 1755, "file_sha256": "39f90bb382ddfee34e808fc93c5a1afafc1d9638a9dc73f2770e815827b4f2ad", "text_sha256": "39f90bb382ddfee34e808fc93c5a1afafc1d9638a9dc73f2770e815827b4f2ad"} [b3-cons-cd381998] Human CD38 is an authentic NAD(P)+ glycohydrolase. (1998). https://pubmed.ncbi.nlm.nih.gov/9494110/ DOI: 10.1042/bj3301383
    Complete structured claim and evidence

  3. Human CD38 hydrolyzes NAD+ to free ADP-ribose and nicotinamide.

    Human CD38 → NAD+ source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    evidence_span
    {"source_cache": "artifacts/niacin-consumption-sources/cd381998.abstract.txt", "locator": "Indexed abstract", "start_char": 0, "end_char": 1755, "file_sha256": "39f90bb382ddfee34e808fc93c5a1afafc1d9638a9dc73f2770e815827b4f2ad", "text_sha256": "39f90bb382ddfee34e808fc93c5a1afafc1d9638a9dc73f2770e815827b4f2ad"}
    experimental_model
    Biochemical characterization of human CD38
    exposure
    NAD+ as substrate
    limitations
    Primary human enzyme study; source abstract used. Product proportions are assay-specific and do not establish tissue flux or supplementation outcomes.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Human
    plain_language
    CD38 can break NAD into ADP-ribose and nicotinamide.
    primary_references
    [b3-cons-cd381998] Human CD38 is an authentic NAD(P)+ glycohydrolase. (1998). https://pubmed.ncbi.nlm.nih.gov/9494110/ DOI: 10.1042/bj3301383
    tissue_or_cell_type
    Cell-free enzyme preparation

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 565–577

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Biochemical characterization of human CD38 · source_derived_draft · unverified_draft

    ### b3-cons-cd38-hydrolysis Human CD38 hydrolyzes NAD+ to free ADP-ribose and nicotinamide. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: CD38 can break NAD into ADP-ribose and nicotinamide. organism: Human tissue_or_cell_type: Cell-free enzyme preparation experimental_model: Biochemical characterization of human CD38 limitations: Primary human enzyme study; source abstract used. Product proportions are assay-specific and do not establish tissue flux or supplementation outcomes. exposure: NAD+ as substrate cross_nutrient: false evidence_span: {"source_cache": "artifacts/niacin-consumption-sources/cd381998.abstract.txt", "locator": "Indexed abstract", "start_char": 0, "end_char": 1755, "file_sha256": "39f90bb382ddfee34e808fc93c5a1afafc1d9638a9dc73f2770e815827b4f2ad", "text_sha256": "39f90bb382ddfee34e808fc93c5a1afafc1d9638a9dc73f2770e815827b4f2ad"} [b3-cons-cd381998] Human CD38 is an authentic NAD(P)+ glycohydrolase. (1998). https://pubmed.ncbi.nlm.nih.gov/9494110/ DOI: 10.1042/bj3301383
    Complete structured claim and evidence

What acts on it

  1. Luteolin inhibited human CD38 at an IC50 below 10 micromolar in vitro.

    Luteolin / 3′,4′,5,7-tetrahydroxyflavone → Human CD38 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human CD38 enzyme assay with docking.
    limitations
    Docking does not prove a binding pose; no human NAD increase or longevity effect established.
    nutrient_topic
    Luteolin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Luteolin / 3′,4′,5,7-tetrahydroxyflavone
    plain_language
    One experimentally inhibited target consumes NAD-related substrates.
    primary_references
    Flavonoids as inhibitors of human CD38. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21641214/ · DOI 10.1016/j.bmcl.2011.05.022

    Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 276–282

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human CD38 enzyme assay with docking. · source_derived_draft · unverified_draft

    ## luteolin-cd38-inhibition One experimentally inhibited target consumes NAD-related substrates. Luteolin inhibited human CD38 at an IC50 below 10 micromolar in vitro. Model: Human CD38 enzyme assay with docking. Limitations: Docking does not prove a binding pose; no human NAD increase or longevity effect established. Evidence access: Primary abstract Flavonoids as inhibitors of human CD38. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21641214/ · DOI 10.1016/j.bmcl.2011.05.022
    Complete structured claim and evidence

  2. CD38 protein abundance increased across 0–1,000 µM boric-acid exposure in DU-145 cells.

    Boric acid / orthoboric acid / B(OH)3 → Human CD38 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/boron-research/18516691.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5fc4f02e11634c2a2d111a99ee4c6175fe8839a8f28152b656b3c29be6745206", "start_char": 0, "end_char": 1733, "text_sha256": "5fc4f02e11634c2a2d111a99ee4c6175fe8839a8f28152b656b3c29be6745206"}
    experimental_model
    Human prostate cancer cell culture and mass spectrometry
    exposure
    Boric acid 100–1,000 µM; methylboronic acid comparator
    limitations
    These are cell-culture exposures, including concentrations far above usual circulating levels. Adduct detection and calcium responses do not prove cancer prevention or direct channel binding.
    nutrient_topic
    Boron research collection; topical membership is not evidence of a direct dietary effect. · Boron
    organism
    Human DU-145 cells; cell-free complex analysis
    plain_language
    The cells increased CD38 protein; more protein does not by itself prove more enzyme activity.
    primary_references
    [boron-p18516691] Boric acid inhibits stored Ca2+ release in DU-145 prostate cancer cells. (2009). https://pubmed.ncbi.nlm.nih.gov/18516691/ DOI: 10.1007/s10565-008-9085-7
    tissue_or_cell_type
    Prostate cancer cells

    Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 287–298

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human prostate cancer cell culture and mass spectrometry · source_derived_draft · unverified_draft

    ### boron-cd38-expression CD38 protein abundance increased across 0–1,000 µM boric-acid exposure in DU-145 cells. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cells increased CD38 protein; more protein does not by itself prove more enzyme activity. organism: Human DU-145 cells; cell-free complex analysis tissue_or_cell_type: Prostate cancer cells experimental_model: Human prostate cancer cell culture and mass spectrometry limitations: These are cell-culture exposures, including concentrations far above usual circulating levels. Adduct detection and calcium responses do not prove cancer prevention or direct channel binding. exposure: Boric acid 100–1,000 µM; methylboronic acid comparator evidence_span: {"source_cache": "artifacts/boron-research/18516691.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5fc4f02e11634c2a2d111a99ee4c6175fe8839a8f28152b656b3c29be6745206", "start_char": 0, "end_char": 1733, "text_sha256": "5fc4f02e11634c2a2d111a99ee4c6175fe8839a8f28152b656b3c29be6745206"} [boron-p18516691] Boric acid inhibits stored Ca2+ release in DU-145 prostate cancer cells. (2009). https://pubmed.ncbi.nlm.nih.gov/18516691/ DOI: 10.1007/s10565-008-9085-7
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Extracellular cyclic ADP-ribose generated by human CD38-expressing COS1 cells was detected by calcium release from sea-urchin egg microsomes.

    Cyclic ADP-ribose → Intracellular calcium-store release source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    true
    evidence_span
    {"source_cache": "artifacts/niacin-consumption-sources/cd381993.abstract.txt", "locator": "Indexed abstract", "start_char": 0, "end_char": 540, "file_sha256": "e8ba405a5300f922bcf34c358d95735b86637331f4cf15a009ac5bf8df93f1e5", "text_sha256": "e8ba405a5300f922bcf34c358d95735b86637331f4cf15a009ac5bf8df93f1e5"}
    experimental_model
    Human CD38 expression in monkey COS1 cells with sea-urchin microsome bioassay
    exposure
    CD38 cDNA transfection; NAD+ extracellular substrate
    limitations
    This mixed-species bioassay does not demonstrate intracellular trafficking of extracellular cADPR or calcium regulation after oral niacin.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Human protein; African green monkey cells; sea urchin microsomes
    plain_language
    A CD38-generated messenger mobilized calcium in an egg-microsome bioassay.
    primary_references
    [b3-cons-cd381993] Human lymphocyte antigen CD38 catalyzes the production of cyclic ADP-ribose. (1993). https://pubmed.ncbi.nlm.nih.gov/8253202/ DOI: 10.1016/0014-5793(93)80735-d
    tissue_or_cell_type
    COS1 kidney-cell culture; sea-urchin egg microsomes

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 607–619

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human CD38 expression in monkey COS1 cells with sea-urchin microsome bioassay · source_derived_draft · unverified_draft

    ### b3-cons-cadpr-store-calcium Extracellular cyclic ADP-ribose generated by human CD38-expressing COS1 cells was detected by calcium release from sea-urchin egg microsomes. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A CD38-generated messenger mobilized calcium in an egg-microsome bioassay. organism: Human protein; African green monkey cells; sea urchin microsomes tissue_or_cell_type: COS1 kidney-cell culture; sea-urchin egg microsomes experimental_model: Human CD38 expression in monkey COS1 cells with sea-urchin microsome bioassay limitations: This mixed-species bioassay does not demonstrate intracellular trafficking of extracellular cADPR or calcium regulation after oral niacin. exposure: CD38 cDNA transfection; NAD+ extracellular substrate cross_nutrient: true evidence_span: {"source_cache": "artifacts/niacin-consumption-sources/cd381993.abstract.txt", "locator": "Indexed abstract", "start_char": 0, "end_char": 540, "file_sha256": "e8ba405a5300f922bcf34c358d95735b86637331f4cf15a009ac5bf8df93f1e5", "text_sha256": "e8ba405a5300f922bcf34c358d95735b86637331f4cf15a009ac5bf8df93f1e5"} [b3-cons-cd381993] Human lymphocyte antigen CD38 catalyzes the production of cyclic ADP-ribose. (1993). https://pubmed.ncbi.nlm.nih.gov/8253202/ DOI: 10.1016/0014-5793(93)80735-d
    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