Component

Human ATR kinase

Study-scoped entity; inspect species, exposure, model and limitations on each claim.

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 acts on it

  1. Caffeine inhibited the checkpoint kinase at concentrations associated with experimental radiosensitization.

    Caffeine → Human ATR kinase source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Kinase assays and irradiated A549 tumor-cell experiments.
    limitations
    Pharmacological radiosensitization context; no claim that dietary caffeine inhibits human DNA repair or treats cancer.
    nutrient_topic
    Caffeine collection; salts, coffee, species and coexposure contexts retain their identities. · Caffeine
    plain_language
    Caffeine also has a laboratory DNA-damage-response target.
    primary_references
    Inhibition of ATM and ATR kinase activities by the radiosensitizing agent, caffeine. · 1999 · https://pubmed.ncbi.nlm.nih.gov/10485486/

    Caffeine: receptors, metabolism, nutrient interactions, adaptation and discovery questions (2026-09-18) · lines 420–426

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Kinase assays and irradiated A549 tumor-cell experiments. · source_derived_draft · unverified_draft

    ## caf-atr Caffeine also has a laboratory DNA-damage-response target. Caffeine inhibited the checkpoint kinase at concentrations associated with experimental radiosensitization. Model: Kinase assays and irradiated A549 tumor-cell experiments. Limitations: Pharmacological radiosensitization context; no claim that dietary caffeine inhibits human DNA repair or treats cancer. Evidence access: Primary abstract Inhibition of ATM and ATR kinase activities by the radiosensitizing agent, caffeine. · 1999 · https://pubmed.ncbi.nlm.nih.gov/10485486/
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. SDH loss increased succinate, impaired aspartate entry into pyrimidine synthesis and produced nucleotide insufficiency with replication stress and increased ATR-inhibitor sensitivity.

    SDH inhibition or loss in human cell models → Pyrimidine production after human-cell SDH impairment source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Human cell genetic/pharmacological SDH perturbations; nucleotide and replication readouts.
    limitations
    Not a clinical treatment recommendation or proof that extra aspartate universally overcomes the competitive block.
    nutrient_topic
    L-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Aspartate
    plain_language
    The effect propagated from metabolism into DNA replication control.
    primary_references
    Succinate dehydrogenase loss suppresses pyrimidine biosynthesis via succinate-mediated inhibition of aspartate transcarbamylase. · 2026 · https://pubmed.ncbi.nlm.nih.gov/42082831/ · DOI 10.1038/s42255-026-01524-w
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Aspartate: redox transfer, nitrogen partitioning and cross-nutrient mechanisms (2026-09-19) · lines 218–224

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human cell genetic/pharmacological SDH perturbations; nucleotide and replication readouts. · source_derived_draft · unverified_draft

    ## l-aspartate-sdh-pyrimidine-stress The effect propagated from metabolism into DNA replication control. SDH loss increased succinate, impaired aspartate entry into pyrimidine synthesis and produced nucleotide insufficiency with replication stress and increased ATR-inhibitor sensitivity. Model: Human cell genetic/pharmacological SDH perturbations; nucleotide and replication readouts. Limitations: Not a clinical treatment recommendation or proof that extra aspartate universally overcomes the competitive block. Evidence access: Primary full text Succinate dehydrogenase loss suppresses pyrimidine biosynthesis via succinate-mediated inhibition of aspartate transcarbamylase. · 2026 · https://pubmed.ncbi.nlm.nih.gov/42082831/ · DOI 10.1038/s42255-026-01524-w
    Complete structured claim and evidence

  2. Caffeine-treated irradiated A549 cells failed G2 arrest and showed radioresistant DNA synthesis after S-phase irradiation.

    Caffeine → DNA-damage-induced cell-cycle checkpoint arrest source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Irradiated cultured A549 lung carcinoma cells.
    limitations
    These findings are not a demonstrated clinical caffeine–radiotherapy benefit.
    nutrient_topic
    Caffeine collection; salts, coffee, species and coexposure contexts retain their identities. · Caffeine
    plain_language
    The cancer-cell experiment measured altered checkpoint behavior.
    primary_references
    Inhibition of ATM and ATR kinase activities by the radiosensitizing agent, caffeine. · 1999 · https://pubmed.ncbi.nlm.nih.gov/10485486/

    Caffeine: receptors, metabolism, nutrient interactions, adaptation and discovery questions (2026-09-18) · lines 428–434

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Irradiated cultured A549 lung carcinoma cells. · source_derived_draft · unverified_draft

    ## caf-checkpoint The cancer-cell experiment measured altered checkpoint behavior. Caffeine-treated irradiated A549 cells failed G2 arrest and showed radioresistant DNA synthesis after S-phase irradiation. Model: Irradiated cultured A549 lung carcinoma cells. Limitations: These findings are not a demonstrated clinical caffeine–radiotherapy benefit. Evidence access: Primary abstract Inhibition of ATM and ATR kinase activities by the radiosensitizing agent, caffeine. · 1999 · https://pubmed.ncbi.nlm.nih.gov/10485486/
    Complete structured claim and evidence

  3. Caffeine reduced radiation-induced p53 Ser15 phosphorylation; DNA-PK was resistant and Chk1 only marginally inhibited in the comparison.

    Caffeine → p53 Ser15 phosphorylation source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Kinase and radiation-response assays.
    limitations
    Do not infer identical activity against all DNA-damage kinases.
    nutrient_topic
    Caffeine collection; salts, coffee, species and coexposure contexts retain their identities. · Caffeine
    plain_language
    The response was selective across the tested kinase pathways.
    primary_references
    Inhibition of ATM and ATR kinase activities by the radiosensitizing agent, caffeine. · 1999 · https://pubmed.ncbi.nlm.nih.gov/10485486/

    Caffeine: receptors, metabolism, nutrient interactions, adaptation and discovery questions (2026-09-18) · lines 436–442

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Kinase and radiation-response assays. · source_derived_draft · unverified_draft

    ## caf-p53 The response was selective across the tested kinase pathways. Caffeine reduced radiation-induced p53 Ser15 phosphorylation; DNA-PK was resistant and Chk1 only marginally inhibited in the comparison. Model: Kinase and radiation-response assays. Limitations: Do not infer identical activity against all DNA-damage kinases. Evidence access: Primary abstract Inhibition of ATM and ATR kinase activities by the radiosensitizing agent, caffeine. · 1999 · https://pubmed.ncbi.nlm.nih.gov/10485486/
    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