Component
Human AP endonuclease 1 / APE1 / APEX1
Context-specific entity; species, compartment and exposure are stated on each claim.
3 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
Omitting MgCl2 abolished detectable APE1 incision in the 2023 control reactions.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Human APE1 delta-N38; standard reaction initiated with 2 mM MgCl2.
- limitations
- Does not prove myricetin inhibits by magnesium chelation or causes magnesium deficiency.
- nutrient_topic
- Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
- plain_language
- The repair enzyme also has a mineral-dependent assay requirement.
- primary_references
- Characterizing inhibitors of human AP endonuclease 1. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36652434/ · DOI 10.1371/journal.pone.0280526
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 676–682
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human APE1 delta-N38; standard reaction initiated with 2 mM MgCl2. · source_derived_draft · unverified_draft
## myricetin-ape1-magnesium The repair enzyme also has a mineral-dependent assay requirement. Omitting MgCl2 abolished detectable APE1 incision in the 2023 control reactions. Model: Human APE1 delta-N38; standard reaction initiated with 2 mM MgCl2. Limitations: Does not prove myricetin inhibits by magnesium chelation or causes magnesium deficiency. Evidence access: Primary full text Characterizing inhibitors of human AP endonuclease 1. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36652434/ · DOI 10.1371/journal.pone.0280526
Complete structured claim and evidenceThe 2009 screen reported potent myricetin inhibition of human APE1; radiotracer follow-up placed IC50 below 0.5 micromolar.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Purified enzyme and fluorescent/radiolabeled abasic-DNA incision assays.
- limitations
- Potency and target specificity were subsequently challenged by aggregation-controlled work; preserve this as a disputed result.
- nutrient_topic
- Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
- plain_language
- An early study identified a candidate DNA-repair inhibitor.
- primary_references
- Identification and characterization of inhibitors of human apurinic/apyrimidinic endonuclease APE1. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19484131/ · DOI 10.1371/journal.pone.0005740
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 652–658
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Purified enzyme and fluorescent/radiolabeled abasic-DNA incision assays. · source_derived_draft · unverified_draft
## myricetin-ape1-original An early study identified a candidate DNA-repair inhibitor. The 2009 screen reported potent myricetin inhibition of human APE1; radiotracer follow-up placed IC50 below 0.5 micromolar. Model: Purified enzyme and fluorescent/radiolabeled abasic-DNA incision assays. Limitations: Potency and target specificity were subsequently challenged by aggregation-controlled work; preserve this as a disputed result. Evidence access: Primary full text Identification and characterization of inhibitors of human apurinic/apyrimidinic endonuclease APE1. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19484131/ · DOI 10.1371/journal.pone.0005740
Complete structured claim and evidenceIn 2023, myricetin showed only weak APE1 inhibition at 0.33 mM with detergent/BSA, preventing an IC50 estimate; inhibition was much stronger without those additives.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Human APE1 delta-N38; UHPLC product assay and dynamic light scattering.
- limitations
- Authors propose nonspecific aggregation as an explanation for earlier potency. This is not a demonstrated explanation for every target in this chapter.
- nutrient_topic
- Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
- plain_language
- Controlling compound aggregation changed the conclusion.
- primary_references
- Characterizing inhibitors of human AP endonuclease 1. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36652434/ · DOI 10.1371/journal.pone.0280526
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 660–666
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human APE1 delta-N38; UHPLC product assay and dynamic light scattering. · source_derived_draft · unverified_draft
## myricetin-ape1-reassessment Controlling compound aggregation changed the conclusion. In 2023, myricetin showed only weak APE1 inhibition at 0.33 mM with detergent/BSA, preventing an IC50 estimate; inhibition was much stronger without those additives. Model: Human APE1 delta-N38; UHPLC product assay and dynamic light scattering. Limitations: Authors propose nonspecific aggregation as an explanation for earlier potency. This is not a demonstrated explanation for every target in this chapter. Evidence access: Primary full text Characterizing inhibitors of human AP endonuclease 1. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36652434/ · DOI 10.1371/journal.pone.0280526
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.