Component

Human ecto-5-prime-nucleotidase / CD73 / NT5E

Context-specific entity; species, compartment and exposure are stated on each claim.

5 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. CD73 knockout did not prevent human cancer cells from using extracellular NAD+ or NMN to restore intracellular NAD+ under the tested conditions.

    Human ecto-5-prime-nucleotidase / CD73 / NT5E → Intracellular NAD restoration from extracellular precursors in human cells source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Human cancer-cell CRISPR knockout and precursor supplementation.
    limitations
    Does not identify a universal alternative uptake route or prove intact NAD crossed the plasma membrane.
    nutrient_topic
    NAD+ collection; molecular form, preparation, species, exposure and manipulation remain explicit. · NAD+
    plain_language
    Cells could still use outside precursor material without CD73.
    primary_references
    Extracellular NAD+ enhances PARP-dependent DNA repair capacity independently of CD73 activity. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31959836/ · DOI 10.1038/s41598-020-57506-9

    NAD+: compartmental supply, consumption and cross-nutrient mechanisms (2026-09-19) · lines 244–250

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human cancer-cell CRISPR knockout and precursor supplementation. · source_derived_draft · unverified_draft

    ## nad-plus-cd73-knockout Cells could still use outside precursor material without CD73. CD73 knockout did not prevent human cancer cells from using extracellular NAD+ or NMN to restore intracellular NAD+ under the tested conditions. Model: Human cancer-cell CRISPR knockout and precursor supplementation. Limitations: Does not identify a universal alternative uptake route or prove intact NAD crossed the plasma membrane. Evidence access: Primary full text Extracellular NAD+ enhances PARP-dependent DNA repair capacity independently of CD73 activity. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31959836/ · DOI 10.1038/s41598-020-57506-9
    Complete structured claim and evidence

  2. Recombinant human CD73 did not process NAD+ and processed NMN poorly in the reported biochemical assays.

    Human ecto-5-prime-nucleotidase / CD73 / NT5E → NMN source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Human recombinant enzyme; biochemical substrate assays.
    limitations
    Do not erase the earlier cellular result. Preparation, assay sensitivity and indirect cellular effects require reconciliation.
    nutrient_topic
    NAD+ collection; molecular form, preparation, species, exposure and manipulation remain explicit. · NAD+
    plain_language
    A later direct assay challenged the proposed precursor-processing enzyme.
    primary_references
    Extracellular NAD+ enhances PARP-dependent DNA repair capacity independently of CD73 activity. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31959836/ · DOI 10.1038/s41598-020-57506-9

    NAD+: compartmental supply, consumption and cross-nutrient mechanisms (2026-09-19) · lines 236–242

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human recombinant enzyme; biochemical substrate assays. · source_derived_draft · unverified_draft

    ## nad-plus-cd73-negative A later direct assay challenged the proposed precursor-processing enzyme. Recombinant human CD73 did not process NAD+ and processed NMN poorly in the reported biochemical assays. Model: Human recombinant enzyme; biochemical substrate assays. Limitations: Do not erase the earlier cellular result. Preparation, assay sensitivity and indirect cellular effects require reconciliation. Evidence access: Primary full text Extracellular NAD+ enhances PARP-dependent DNA repair capacity independently of CD73 activity. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31959836/ · DOI 10.1038/s41598-020-57506-9
    Complete structured claim and evidence

  3. CD73 silencing or pharmacological inhibition reduced NMN-supported survival after NAMPT inhibition in human tumor cells; the authors assigned CD73 a role in converting extracellular NMN to NR.

    Human ecto-5-prime-nucleotidase / CD73 / NT5E → Nicotinamide riboside source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human tumor-cell CD73 overexpression/silencing and FK866 experiments.
    limitations
    Mechanistic assignment is disputed by the later human recombinant-enzyme and knockout study. Primary abstract accessed here; direct catalytic attribution is retained as reported.
    nutrient_topic
    NAD+ collection; molecular form, preparation, species, exposure and manipulation remain explicit. · NAD+
    plain_language
    One study found that CD73 helped cells use an outside NAD precursor.
    primary_references
    CD73 protein as a source of extracellular precursors for sustained NAD+ biosynthesis in FK866-treated tumor cells. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23880765/ · DOI 10.1074/jbc.M113.470435

    NAD+: compartmental supply, consumption and cross-nutrient mechanisms (2026-09-19) · lines 228–234

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human tumor-cell CD73 overexpression/silencing and FK866 experiments. · source_derived_draft · unverified_draft

    ## nad-plus-cd73-positive One study found that CD73 helped cells use an outside NAD precursor. CD73 silencing or pharmacological inhibition reduced NMN-supported survival after NAMPT inhibition in human tumor cells; the authors assigned CD73 a role in converting extracellular NMN to NR. Model: Human tumor-cell CD73 overexpression/silencing and FK866 experiments. Limitations: Mechanistic assignment is disputed by the later human recombinant-enzyme and knockout study. Primary abstract accessed here; direct catalytic attribution is retained as reported. Evidence access: Primary abstract CD73 protein as a source of extracellular precursors for sustained NAD+ biosynthesis in FK866-treated tumor cells. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23880765/ · DOI 10.1074/jbc.M113.470435
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Extracellular NAD+ or NMN restored intracellular NAD availability, PAR-dependent signaling and XRCC1 recruitment in the tested NAD-depleted human cells independently of CD73 status.

    NAD+ → NAD-dependent XRCC1 recruitment and PAR signaling in human cells source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Human MCF-7 cells with NAMPT inhibition, CD73 comparison and serum-containing medium; NMN/NR XRCC1 rescue is reported as data not shown.
    limitations
    Rescue depended on medium and incubation time; serum-free and heat-inactivated-serum conditions did not give the same early rescue. No proof of intact cellular NAD uptake or clinical benefit.
    nutrient_topic
    NAD+ collection; molecular form, preparation, species, exposure and manipulation remain explicit. · NAD+
    plain_language
    Supplying precursor material restored part of a repair response in this model.
    primary_references
    Extracellular NAD+ enhances PARP-dependent DNA repair capacity independently of CD73 activity. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31959836/ · DOI 10.1038/s41598-020-57506-9

    NAD+: compartmental supply, consumption and cross-nutrient mechanisms (2026-09-19) · lines 260–266

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human MCF-7 cells with NAMPT inhibition, CD73 comparison and serum-containing medium; NMN/NR XRCC1 rescue is reported as data not shown. · source_derived_draft · unverified_draft

    ## nad-plus-repair-precursor-rescue Supplying precursor material restored part of a repair response in this model. Extracellular NAD+ or NMN restored intracellular NAD availability, PAR-dependent signaling and XRCC1 recruitment in the tested NAD-depleted human cells independently of CD73 status. Model: Human MCF-7 cells with NAMPT inhibition, CD73 comparison and serum-containing medium; NMN/NR XRCC1 rescue is reported as data not shown. Limitations: Rescue depended on medium and incubation time; serum-free and heat-inactivated-serum conditions did not give the same early rescue. No proof of intact cellular NAD uptake or clinical benefit. Evidence access: Primary full text Extracellular NAD+ enhances PARP-dependent DNA repair capacity independently of CD73 activity. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31959836/ · DOI 10.1038/s41598-020-57506-9
    Complete structured claim and evidence

  2. NAD+ restored XRCC1 recruitment in NAD-depleted MCF-7 cells more readily in fetal-bovine-serum-containing medium than serum-free or heat-inactivated-serum conditions; precursor metabolism and rescue also depended on incubation time.

    NAD precursor processing by fetal bovine serum → NAD-dependent XRCC1 recruitment and PAR signaling in human cells source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Human cells; medium comparison, NMR precursor stability and six- versus 24-hour exposure.
    limitations
    Serum components are not individually identified by this result; do not assign the effect to human CD73 or infer direct uptake.
    nutrient_topic
    NAD+ collection; molecular form, preparation, species, exposure and manipulation remain explicit. · NAD+
    plain_language
    The material outside a cell can determine whether an added precursor works.
    primary_references
    Extracellular NAD+ enhances PARP-dependent DNA repair capacity independently of CD73 activity. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31959836/ · DOI 10.1038/s41598-020-57506-9

    NAD+: compartmental supply, consumption and cross-nutrient mechanisms (2026-09-19) · lines 364–370

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human cells; medium comparison, NMR precursor stability and six- versus 24-hour exposure. · source_derived_draft · unverified_draft

    ## nad-plus-serum-processing The material outside a cell can determine whether an added precursor works. NAD+ restored XRCC1 recruitment in NAD-depleted MCF-7 cells more readily in fetal-bovine-serum-containing medium than serum-free or heat-inactivated-serum conditions; precursor metabolism and rescue also depended on incubation time. Model: Human cells; medium comparison, NMR precursor stability and six- versus 24-hour exposure. Limitations: Serum components are not individually identified by this result; do not assign the effect to human CD73 or infer direct uptake. Evidence access: Primary full text Extracellular NAD+ enhances PARP-dependent DNA repair capacity independently of CD73 activity. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31959836/ · DOI 10.1038/s41598-020-57506-9
    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