Component

Human nicotinamide phosphoribosyltransferase / NAMPT

Human nicotinamide salvage enzyme; NMPRTase, PBEF, visfatin.

11 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. NAD depletion with NAMPT inhibitor STF-118804 abolished resveratrol-mediated induction of BRCA1, FOXO3A, NAMPT, SESN2 and SIRT6 in human HeLa cells.

    Human nicotinamide phosphoribosyltransferase / NAMPT → Resveratrol-induced stress-protein response in human HeLa cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Pharmacological NAMPT inhibition.
    limitations
    This does not prove supplementation with niacin, NR or NMN improves the response.
    nutrient_topic
    Resveratrol collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Resveratrol
    plain_language
    The response needs functioning NAD salvage machinery.
    primary_references
    A human tRNA synthetase is a potent PARP1-activating effector target for resveratrol. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25533949/ · DOI 10.1038/nature14028
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Resveratrol: metabolites, target selectivity and cross-nutrient mechanisms (2026-09-19) · lines 334–340

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Pharmacological NAMPT inhibition. · source_derived_draft · unverified_draft

    ## resveratrol-nampt-block The response needs functioning NAD salvage machinery. NAD depletion with NAMPT inhibitor STF-118804 abolished resveratrol-mediated induction of BRCA1, FOXO3A, NAMPT, SESN2 and SIRT6 in human HeLa cells. Model: Pharmacological NAMPT inhibition. Limitations: This does not prove supplementation with niacin, NR or NMN improves the response. Evidence access: Primary full text A human tRNA synthetase is a potent PARP1-activating effector target for resveratrol. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25533949/ · DOI 10.1038/nature14028
    Complete structured claim and evidence

  2. NAMPT-supported NAD metabolism sustained glycolysis and respiration and promoted a proinflammatory SASP through the AMPK–p53–p38/NF-kappaB regulatory network in the tested senescent cells.

    Human nicotinamide phosphoribosyltransferase / NAMPT → Proinflammatory SASP in human IMR90 fibroblasts source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Human IMR90 fibroblast senescence; NAMPT inhibition and knockdown.
    limitations
    Not proof that NAD supplementation causes cancer in humans or that all senescent cells respond alike.
    nutrient_topic
    NAD+ collection; molecular form, preparation, species, exposure and manipulation remain explicit. · NAD+
    plain_language
    Supporting cellular metabolism can also support inflammatory secretion.
    primary_references
    NAD+ metabolism governs the proinflammatory senescence-associated secretome. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30778219/ · DOI 10.1038/s41556-019-0287-4

    NAD+: compartmental supply, consumption and cross-nutrient mechanisms (2026-09-19) · lines 156–162

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human IMR90 fibroblast senescence; NAMPT inhibition and knockdown. · source_derived_draft · unverified_draft

    ## nad-plus-nampt-sasp Supporting cellular metabolism can also support inflammatory secretion. NAMPT-supported NAD metabolism sustained glycolysis and respiration and promoted a proinflammatory SASP through the AMPK–p53–p38/NF-kappaB regulatory network in the tested senescent cells. Model: Human IMR90 fibroblast senescence; NAMPT inhibition and knockdown. Limitations: Not proof that NAD supplementation causes cancer in humans or that all senescent cells respond alike. Evidence access: Primary full text NAD+ metabolism governs the proinflammatory senescence-associated secretome. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30778219/ · DOI 10.1038/s41556-019-0287-4
    Complete structured claim and evidence

  3. FK866-mediated NAD depletion impaired DNA repair and damage-induced PARylation in the tested human cancer-cell experiments.

    Human nicotinamide phosphoribosyltransferase / NAMPT → DNA repair after NAD depletion in human MCF-7 cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Human MCF-7 cells, NAMPT inhibitor, genotoxins and CometChip/PAR assays.
    limitations
    Genotoxin and endpoint dependent; not proof that raising NAD prevents human cancer.
    nutrient_topic
    NAD+ collection; molecular form, preparation, species, exposure and manipulation remain explicit. · NAD+
    plain_language
    When salvage is blocked, repair enzymes can lose access to their substrate.
    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
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    NAD+: compartmental supply, consumption and cross-nutrient mechanisms (2026-09-19) · lines 252–258

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human MCF-7 cells, NAMPT inhibitor, genotoxins and CometChip/PAR assays. · source_derived_draft · unverified_draft

    ## nad-plus-repair-depletion When salvage is blocked, repair enzymes can lose access to their substrate. FK866-mediated NAD depletion impaired DNA repair and damage-induced PARylation in the tested human cancer-cell experiments. Model: Human MCF-7 cells, NAMPT inhibitor, genotoxins and CometChip/PAR assays. Limitations: Genotoxin and endpoint dependent; not proof that raising NAD prevents human cancer. 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

  4. FK866 inhibition of NAMPT depleted nuclear and cytoplasmic free NAD+ with approximate two-hour half-times, versus approximately eight hours in mitochondria; 16 hours reduced free NAD+ by over 85% in all three compartments.

    Human nicotinamide phosphoribosyltransferase / NAMPT → Free NAD+ pools in human HEK293T compartments source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Cultured human-cell biosensor experiments.
    limitations
    Drug-induced loss does not define dietary niacin deficiency or establish equivalent depletion in every tissue.
    nutrient_topic
    NAD+ collection; molecular form, preparation, species, exposure and manipulation remain explicit. · NAD+
    plain_language
    Blocking recycling empties NAD pools at different speeds.
    primary_references
    Biosensor reveals multiple sources for mitochondrial NAD⁺. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27313049/ · DOI 10.1126/science.aad5168
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    NAD+: compartmental supply, consumption and cross-nutrient mechanisms (2026-09-19) · lines 20–26

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Cultured human-cell biosensor experiments. · source_derived_draft · unverified_draft

    ## nad-plus-salvage-depletion Blocking recycling empties NAD pools at different speeds. FK866 inhibition of NAMPT depleted nuclear and cytoplasmic free NAD+ with approximate two-hour half-times, versus approximately eight hours in mitochondria; 16 hours reduced free NAD+ by over 85% in all three compartments. Model: Cultured human-cell biosensor experiments. Limitations: Drug-induced loss does not define dietary niacin deficiency or establish equivalent depletion in every tissue. Evidence access: Primary full text Biosensor reveals multiple sources for mitochondrial NAD⁺. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27313049/ · DOI 10.1126/science.aad5168
    Complete structured claim and evidence

  5. Human NAMPT converts nicotinamide and PRPP to nicotinamide mononucleotide and pyrophosphate.

    Human nicotinamide phosphoribosyltransferase / NAMPT → NMN source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/niacin-precursors-sources/nampt2009.abstract.txt", "locator": "Indexed primary abstract", "start_char": 0, "end_char": 1272, "file_sha256": "b67ca4decafccfc4132deba87ffddf2114e60542c77fa4354165d414aa0f13c5", "text_sha256": "b67ca4decafccfc4132deba87ffddf2114e60542c77fa4354165d414aa0f13c5"}
    experimental_model
    Purified human NAMPT reaction monitoring by 1H/31P NMR and substrate/product crystallography
    exposure
    Biochemical or structural assay; no dietary intervention
    limitations
    Purified-enzyme evidence does not establish dietary intake requirements or clinical outcomes.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Homo sapiens
    plain_language
    Nicotinamide salvage first makes NMN.
    primary_references
    [b3-pre-nampt2009] Structure and reaction mechanism of human nicotinamide phosphoribosyltransferase. (2010). https://pubmed.ncbi.nlm.nih.gov/19819904/ DOI: 10.1093/jb/mvp152
    tissue_or_cell_type
    Purified recombinant protein; no intact tissue

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 369–380

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified human NAMPT reaction monitoring by 1H/31P NMR and substrate/product crystallography · source_derived_draft · unverified_draft

    ### b3-pre-nampt-reaction Human NAMPT converts nicotinamide and PRPP to nicotinamide mononucleotide and pyrophosphate. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Nicotinamide salvage first makes NMN. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Purified human NAMPT reaction monitoring by 1H/31P NMR and substrate/product crystallography limitations: Purified-enzyme evidence does not establish dietary intake requirements or clinical outcomes. exposure: Biochemical or structural assay; no dietary intervention evidence_span: {"source_cache": "artifacts/niacin-precursors-sources/nampt2009.abstract.txt", "locator": "Indexed primary abstract", "start_char": 0, "end_char": 1272, "file_sha256": "b67ca4decafccfc4132deba87ffddf2114e60542c77fa4354165d414aa0f13c5", "text_sha256": "b67ca4decafccfc4132deba87ffddf2114e60542c77fa4354165d414aa0f13c5"} [b3-pre-nampt2009] Structure and reaction mechanism of human nicotinamide phosphoribosyltransferase. (2010). https://pubmed.ncbi.nlm.nih.gov/19819904/ DOI: 10.1093/jb/mvp152
    Complete structured claim and evidence

  6. NMR monitoring demonstrated reversibility of the purified human NAMPT reaction; the measured equilibrium constant was 0.14 under the study conditions.

    Human nicotinamide phosphoribosyltransferase / NAMPT → NMN source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/niacin-precursors-sources/nampt2009.abstract.txt", "locator": "Indexed primary abstract", "start_char": 0, "end_char": 1272, "file_sha256": "b67ca4decafccfc4132deba87ffddf2114e60542c77fa4354165d414aa0f13c5", "text_sha256": "b67ca4decafccfc4132deba87ffddf2114e60542c77fa4354165d414aa0f13c5"}
    experimental_model
    Purified human NAMPT reaction monitoring by 1H/31P NMR and substrate/product crystallography
    exposure
    Biochemical or structural assay; no dietary intervention
    limitations
    An isolated reaction equilibrium does not establish net intracellular salvage flux.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Homo sapiens
    plain_language
    This isolated chemical reaction can run in either direction.
    primary_references
    [b3-pre-nampt2009] Structure and reaction mechanism of human nicotinamide phosphoribosyltransferase. (2010). https://pubmed.ncbi.nlm.nih.gov/19819904/ DOI: 10.1093/jb/mvp152
    tissue_or_cell_type
    Purified recombinant protein; no intact tissue

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 382–393

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified human NAMPT reaction monitoring by 1H/31P NMR and substrate/product crystallography · source_derived_draft · unverified_draft

    ### b3-pre-nampt-reversible NMR monitoring demonstrated reversibility of the purified human NAMPT reaction; the measured equilibrium constant was 0.14 under the study conditions. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: This isolated chemical reaction can run in either direction. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Purified human NAMPT reaction monitoring by 1H/31P NMR and substrate/product crystallography limitations: An isolated reaction equilibrium does not establish net intracellular salvage flux. exposure: Biochemical or structural assay; no dietary intervention evidence_span: {"source_cache": "artifacts/niacin-precursors-sources/nampt2009.abstract.txt", "locator": "Indexed primary abstract", "start_char": 0, "end_char": 1272, "file_sha256": "b67ca4decafccfc4132deba87ffddf2114e60542c77fa4354165d414aa0f13c5", "text_sha256": "b67ca4decafccfc4132deba87ffddf2114e60542c77fa4354165d414aa0f13c5"} [b3-pre-nampt2009] Structure and reaction mechanism of human nicotinamide phosphoribosyltransferase. (2010). https://pubmed.ncbi.nlm.nih.gov/19819904/ DOI: 10.1093/jb/mvp152
    Complete structured claim and evidence

What acts on it

  1. HMGA1-dependent NAMPT expression contributed to increased NAD metabolism and the proinflammatory secretory phenotype in oncogene-induced senescent human IMR90 fibroblasts.

    Human HMGA1 → Human nicotinamide phosphoribosyltransferase / NAMPT source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Human fibroblast oncogene-induced senescence with genetic perturbations.
    limitations
    Senescence type matters; replicative and mitochondrial-dysfunction senescence need not share this pattern.
    nutrient_topic
    NAD+ collection; molecular form, preparation, species, exposure and manipulation remain explicit. · NAD+
    plain_language
    A gene regulator can increase NAD salvage in a cell that is already senescent.
    primary_references
    NAD+ metabolism governs the proinflammatory senescence-associated secretome. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30778219/ · DOI 10.1038/s41556-019-0287-4

    NAD+: compartmental supply, consumption and cross-nutrient mechanisms (2026-09-19) · lines 148–154

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human fibroblast oncogene-induced senescence with genetic perturbations. · source_derived_draft · unverified_draft

    ## nad-plus-hmga-nampt A gene regulator can increase NAD salvage in a cell that is already senescent. HMGA1-dependent NAMPT expression contributed to increased NAD metabolism and the proinflammatory secretory phenotype in oncogene-induced senescent human IMR90 fibroblasts. Model: Human fibroblast oncogene-induced senescence with genetic perturbations. Limitations: Senescence type matters; replicative and mitochondrial-dysfunction senescence need not share this pattern. Evidence access: Primary full text NAD+ metabolism governs the proinflammatory senescence-associated secretome. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30778219/ · DOI 10.1038/s41556-019-0287-4
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. In nonobese postmenopausal women with normal glucose tolerance, 75 mg/day resveratrol for 12 weeks did not improve liver, muscle or adipose insulin sensitivity or measured AMPK/SIRT1/NAMPT/PPARGC1A targets.

    Resveratrol → Metabolic outcomes in nonobese postmenopausal women source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Randomized double-blind placebo-controlled trial.
    limitations
    Null result is population- and regimen-specific.
    nutrient_topic
    Resveratrol collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Resveratrol
    plain_language
    Effects in metabolically abnormal models do not automatically transfer to healthy people.
    primary_references
    Resveratrol supplementation does not improve metabolic function in nonobese women with normal glucose tolerance. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23102619/ · DOI 10.1016/j.cmet.2012.09.015

    Resveratrol: metabolites, target selectivity and cross-nutrient mechanisms (2026-09-19) · lines 470–476

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Randomized double-blind placebo-controlled trial. · source_derived_draft · unverified_draft

    ## resveratrol-human-women-null Effects in metabolically abnormal models do not automatically transfer to healthy people. In nonobese postmenopausal women with normal glucose tolerance, 75 mg/day resveratrol for 12 weeks did not improve liver, muscle or adipose insulin sensitivity or measured AMPK/SIRT1/NAMPT/PPARGC1A targets. Model: Randomized double-blind placebo-controlled trial. Limitations: Null result is population- and regimen-specific. Evidence access: Primary abstract Resveratrol supplementation does not improve metabolic function in nonobese women with normal glucose tolerance. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23102619/ · DOI 10.1016/j.cmet.2012.09.015
    Complete structured claim and evidence

  2. 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

  3. Removing bacterial PncA abolished, and supplying it enabled, bacterial protection against NAMPT inhibitors in the tested cancer-cell and xenograft systems.

    Escherichia coli nicotinamidase PncA → NAMPT-inhibitor-induced cancer-cell killing source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Microbial genetic manipulation plus mammalian cancer models.
    limitations
    Preclinical resistance mechanism, not guidance to manipulate microbiota during cancer treatment.
    nutrient_topic
    NAD+ collection; molecular form, preparation, species, exposure and manipulation remain explicit. · NAD+
    plain_language
    An alternative precursor source can defeat a blockade of salvage.
    primary_references
    Bacteria Boost Mammalian Host NAD Metabolism by Engaging the Deamidated Biosynthesis Pathway. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32130883/ · DOI 10.1016/j.cmet.2020.02.001
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    NAD+: compartmental supply, consumption and cross-nutrient mechanisms (2026-09-19) · lines 172–178

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Microbial genetic manipulation plus mammalian cancer models. · source_derived_draft · unverified_draft

    ## nad-plus-microbial-rescue An alternative precursor source can defeat a blockade of salvage. Removing bacterial PncA abolished, and supplying it enabled, bacterial protection against NAMPT inhibitors in the tested cancer-cell and xenograft systems. Model: Microbial genetic manipulation plus mammalian cancer models. Limitations: Preclinical resistance mechanism, not guidance to manipulate microbiota during cancer treatment. Evidence access: Primary full text Bacteria Boost Mammalian Host NAD Metabolism by Engaging the Deamidated Biosynthesis Pathway. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32130883/ · DOI 10.1016/j.cmet.2020.02.001
    Complete structured claim and evidence

  4. The PARP inhibitor Tiq-A slowed early nuclear/cytoplasmic NAD+ depletion after NAMPT inhibition, with little effect on mitochondrial depletion.

    Human PARP1 → Nucleocytoplasmic NAD depletion during salvage blockade source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Cultured human cells; pharmacological PARP inhibition.
    limitations
    Tiq-A is not a PARP1-specific genetic experiment, and did not prevent eventual depletion in all compartments.
    nutrient_topic
    NAD+ collection; molecular form, preparation, species, exposure and manipulation remain explicit. · NAD+
    plain_language
    Consumption can determine how quickly a blocked supply becomes a shortage.
    primary_references
    Biosensor reveals multiple sources for mitochondrial NAD⁺. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27313049/ · DOI 10.1126/science.aad5168
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    NAD+: compartmental supply, consumption and cross-nutrient mechanisms (2026-09-19) · lines 28–34

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Cultured human cells; pharmacological PARP inhibition. · source_derived_draft · unverified_draft

    ## nad-plus-parp-depletion-rate Consumption can determine how quickly a blocked supply becomes a shortage. The PARP inhibitor Tiq-A slowed early nuclear/cytoplasmic NAD+ depletion after NAMPT inhibition, with little effect on mitochondrial depletion. Model: Cultured human cells; pharmacological PARP inhibition. Limitations: Tiq-A is not a PARP1-specific genetic experiment, and did not prevent eventual depletion in all compartments. Evidence access: Primary full text Biosensor reveals multiple sources for mitochondrial NAD⁺. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27313049/ · DOI 10.1126/science.aad5168
    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