Component

Human ATM kinase

Human ATM kinase. Species, exposure and limitations are retained in each linked claim.

7 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. DIM rapidly activated ATM and enhanced ATM-linked DNA-damage-response signaling in the studied cell system.

    3,3'-Diindolylmethane / DIM → Human ATM kinase source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/dim-research/24127581.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6e938b73271132ed6dc4ed9f3a4d7bb6cf85fd3071df159c17c9fcef93b901fc", "start_char": 0, "end_char": 1379, "text_sha256": "6e938b73271132ed6dc4ed9f3a4d7bb6cf85fd3071df159c17c9fcef93b901fc"}
    experimental_model
    Cell signaling and rodent radiation experiments
    exposure
    Submicromolar cell exposures and multidose rodent DIM schedules
    limitations
    No human radioprotection trial. Lack of protection in tested tumor xenografts cannot establish safety with all radiotherapy or cancer types.
    nutrient_topic
    Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. · 3,3'-Diindolylmethane / DIM
    organism
    Cultured cells and irradiated rodents; breast-tumor xenografts separately
    plain_language
    The compound also affected a DNA-damage sensor.
    primary_references
    [dim-p24127581] DIM (3,3'-diindolylmethane) confers protection against ionizing radiation by a unique mechanism. (2013). https://pubmed.ncbi.nlm.nih.gov/24127581/ DOI: 10.1073/pnas.1308206110
    tissue_or_cell_type
    ATM-mediated damage response

    Diindolylmethane (DIM): formation, receptor signaling, metabolism and drug interactions (2026-09-17) · lines 1429–1440

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell signaling and rodent radiation experiments · source_derived_draft · unverified_draft

    ### dim-atm-response DIM rapidly activated ATM and enhanced ATM-linked DNA-damage-response signaling in the studied cell system. Condition category: normal nutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The compound also affected a DNA-damage sensor. organism: Cultured cells and irradiated rodents; breast-tumor xenografts separately tissue_or_cell_type: ATM-mediated damage response experimental_model: Cell signaling and rodent radiation experiments limitations: No human radioprotection trial. Lack of protection in tested tumor xenografts cannot establish safety with all radiotherapy or cancer types. exposure: Submicromolar cell exposures and multidose rodent DIM schedules evidence_span: {"source_cache": "artifacts/dim-research/24127581.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6e938b73271132ed6dc4ed9f3a4d7bb6cf85fd3071df159c17c9fcef93b901fc", "start_char": 0, "end_char": 1379, "text_sha256": "6e938b73271132ed6dc4ed9f3a4d7bb6cf85fd3071df159c17c9fcef93b901fc"} [dim-p24127581] DIM (3,3'-diindolylmethane) confers protection against ionizing radiation by a unique mechanism. (2013). https://pubmed.ncbi.nlm.nih.gov/24127581/ DOI: 10.1073/pnas.1308206110
    Complete structured claim and evidence

  2. Ascorbate restoration prevented Cr(VI)-induced ATM activation observed in standard ascorbate-poor human lung-cell cultures.

    L-Ascorbate → Human ATM kinase source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/chromium-research/25977998.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3", "start_char": 0, "end_char": 2163, "text_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3"}
    experimental_model
    Ascorbate restoration and ATM perturbation in human lung-cell cultures
    exposure
    Chromate exposure in standard ascorbate-poor versus ascorbate-restored cells; ATM inhibition/silencing
    limitations
    Cr(VI) toxicology, not an experiment with dietary Cr(III). Loss of ATM activation does not mean loss of all genotoxicity or that vitamin C universally detoxifies chromium.
    nutrient_topic
    Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
    organism
    Human H460 cells and normal lung fibroblasts
    plain_language
    Vitamin C availability changed which damage-response pathway the toxic exposure activated.
    primary_references
    [chromium-p25977998] Different ATM Signaling in Response to Chromium(VI) Metabolism via Ascorbate and Nonascorbate Reduction: Implications for in Vitro Models and Toxicogenomics. (2016). https://pubmed.ncbi.nlm.nih.gov/25977998/ DOI: 10.1289/ehp.1409434
    tissue_or_cell_type
    DNA-damage signaling
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 1121–1132

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ascorbate restoration and ATM perturbation in human lung-cell cultures · source_derived_draft · unverified_draft

    ### chromium-ascorbate-atm-context Ascorbate restoration prevented Cr(VI)-induced ATM activation observed in standard ascorbate-poor human lung-cell cultures. Condition category: nutrient_deficiency nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin C availability changed which damage-response pathway the toxic exposure activated. organism: Human H460 cells and normal lung fibroblasts tissue_or_cell_type: DNA-damage signaling experimental_model: Ascorbate restoration and ATM perturbation in human lung-cell cultures limitations: Cr(VI) toxicology, not an experiment with dietary Cr(III). Loss of ATM activation does not mean loss of all genotoxicity or that vitamin C universally detoxifies chromium. exposure: Chromate exposure in standard ascorbate-poor versus ascorbate-restored cells; ATM inhibition/silencing evidence_span: {"source_cache": "artifacts/chromium-research/25977998.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3", "start_char": 0, "end_char": 2163, "text_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3"} [chromium-p25977998] Different ATM Signaling in Response to Chromium(VI) Metabolism via Ascorbate and Nonascorbate Reduction: Implications for in Vitro Models and Toxicogenomics. (2016). https://pubmed.ncbi.nlm.nih.gov/25977998/ DOI: 10.1289/ehp.1409434
    Complete structured claim and evidence

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

    Caffeine → Human ATM 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 412–418

    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-atm 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. Chromate exposure induced CHK2 phosphorylation as part of the ATM response in standard ascorbate-poor human cell cultures.

    Chromate / chromium(VI) oxyanion → Human checkpoint kinase 2 / CHEK2 source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/chromium-research/25977998.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3", "start_char": 0, "end_char": 2163, "text_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3"}
    experimental_model
    Ascorbate restoration and ATM perturbation in human lung-cell cultures
    exposure
    Chromate exposure in standard ascorbate-poor versus ascorbate-restored cells; ATM inhibition/silencing
    limitations
    Cr(VI) toxicology, not an experiment with dietary Cr(III). Loss of ATM activation does not mean loss of all genotoxicity or that vitamin C universally detoxifies chromium.
    nutrient_topic
    Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
    organism
    Human H460 cells and normal lung fibroblasts
    plain_language
    This downstream damage-response protein changed in the low-ascorbate culture condition.
    primary_references
    [chromium-p25977998] Different ATM Signaling in Response to Chromium(VI) Metabolism via Ascorbate and Nonascorbate Reduction: Implications for in Vitro Models and Toxicogenomics. (2016). https://pubmed.ncbi.nlm.nih.gov/25977998/ DOI: 10.1289/ehp.1409434
    tissue_or_cell_type
    DNA-damage signaling
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 1134–1145

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ascorbate restoration and ATM perturbation in human lung-cell cultures · source_derived_draft · unverified_draft

    ### chromium-chromate-chk2 Chromate exposure induced CHK2 phosphorylation as part of the ATM response in standard ascorbate-poor human cell cultures. Condition category: nutrient_deficiency nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This downstream damage-response protein changed in the low-ascorbate culture condition. organism: Human H460 cells and normal lung fibroblasts tissue_or_cell_type: DNA-damage signaling experimental_model: Ascorbate restoration and ATM perturbation in human lung-cell cultures limitations: Cr(VI) toxicology, not an experiment with dietary Cr(III). Loss of ATM activation does not mean loss of all genotoxicity or that vitamin C universally detoxifies chromium. exposure: Chromate exposure in standard ascorbate-poor versus ascorbate-restored cells; ATM inhibition/silencing evidence_span: {"source_cache": "artifacts/chromium-research/25977998.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3", "start_char": 0, "end_char": 2163, "text_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3"} [chromium-p25977998] Different ATM Signaling in Response to Chromium(VI) Metabolism via Ascorbate and Nonascorbate Reduction: Implications for in Vitro Models and Toxicogenomics. (2016). https://pubmed.ncbi.nlm.nih.gov/25977998/ DOI: 10.1289/ehp.1409434
    Complete structured claim and evidence

  2. Chromate exposure induced KAP1 phosphorylation as part of the ATM response in standard ascorbate-poor human cell cultures.

    Chromate / chromium(VI) oxyanion → Human KAP1 / TRIM28 source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/chromium-research/25977998.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3", "start_char": 0, "end_char": 2163, "text_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3"}
    experimental_model
    Ascorbate restoration and ATM perturbation in human lung-cell cultures
    exposure
    Chromate exposure in standard ascorbate-poor versus ascorbate-restored cells; ATM inhibition/silencing
    limitations
    Cr(VI) toxicology, not an experiment with dietary Cr(III). Loss of ATM activation does not mean loss of all genotoxicity or that vitamin C universally detoxifies chromium.
    nutrient_topic
    Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
    organism
    Human H460 cells and normal lung fibroblasts
    plain_language
    This downstream damage-response protein changed in the low-ascorbate culture condition.
    primary_references
    [chromium-p25977998] Different ATM Signaling in Response to Chromium(VI) Metabolism via Ascorbate and Nonascorbate Reduction: Implications for in Vitro Models and Toxicogenomics. (2016). https://pubmed.ncbi.nlm.nih.gov/25977998/ DOI: 10.1289/ehp.1409434
    tissue_or_cell_type
    DNA-damage signaling
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 1147–1158

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ascorbate restoration and ATM perturbation in human lung-cell cultures · source_derived_draft · unverified_draft

    ### chromium-chromate-kap1 Chromate exposure induced KAP1 phosphorylation as part of the ATM response in standard ascorbate-poor human cell cultures. Condition category: nutrient_deficiency nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This downstream damage-response protein changed in the low-ascorbate culture condition. organism: Human H460 cells and normal lung fibroblasts tissue_or_cell_type: DNA-damage signaling experimental_model: Ascorbate restoration and ATM perturbation in human lung-cell cultures limitations: Cr(VI) toxicology, not an experiment with dietary Cr(III). Loss of ATM activation does not mean loss of all genotoxicity or that vitamin C universally detoxifies chromium. exposure: Chromate exposure in standard ascorbate-poor versus ascorbate-restored cells; ATM inhibition/silencing evidence_span: {"source_cache": "artifacts/chromium-research/25977998.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3", "start_char": 0, "end_char": 2163, "text_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3"} [chromium-p25977998] Different ATM Signaling in Response to Chromium(VI) Metabolism via Ascorbate and Nonascorbate Reduction: Implications for in Vitro Models and Toxicogenomics. (2016). https://pubmed.ncbi.nlm.nih.gov/25977998/ DOI: 10.1289/ehp.1409434
    Complete structured claim and evidence

  3. 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

  4. 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