Component

Human unc-51-like autophagy activating kinase ULK1

Human unc-51-like autophagy activating kinase ULK1. Species, exposure and limitations are retained in each linked claim.

2 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. Copper-binding-disruptive ULK1 mutations reduced autophagy signaling and autophagosome formation in the tested cells.

    Human unc-51-like autophagy activating kinase ULK1 → Autophagosome formation source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/copper-research/32203415.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f248044309434e00cd35941d0e525a9c73a07e8d78eead20f7d7b6bdcb5f2915", "start_char": 0, "end_char": 1077, "text_sha256": "f248044309434e00cd35941d0e525a9c73a07e8d78eead20f7d7b6bdcb5f2915"}
    experimental_model
    Recombinant kinase assays, genetic perturbations and lung tumor models
    exposure
    Copper exposure, copper-binding mutations and Ctr1 deletion
    limitations
    Preclinical molecular evidence; not proof that copper supplementation improves autophagy in healthy people or that chelation improves cancer survival.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Human recombinant ULK1/ULK2 with complementary mouse systems
    plain_language
    A binding defect interrupted the recycling pathway downstream.
    primary_references
    [copper-p32203415] Copper is an essential regulator of the autophagic kinases ULK1/2 to drive lung adenocarcinoma. (2020). https://pubmed.ncbi.nlm.nih.gov/32203415/ DOI: 10.1038/s41556-020-0481-4
    tissue_or_cell_type
    Autophagy signaling

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 1261–1272

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant kinase assays, genetic perturbations and lung tumor models · source_derived_draft · unverified_draft

    ### copper-ulk1-copper-autophagy Copper-binding-disruptive ULK1 mutations reduced autophagy signaling and autophagosome formation in the tested cells. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: A binding defect interrupted the recycling pathway downstream. organism: Human recombinant ULK1/ULK2 with complementary mouse systems tissue_or_cell_type: Autophagy signaling experimental_model: Recombinant kinase assays, genetic perturbations and lung tumor models limitations: Preclinical molecular evidence; not proof that copper supplementation improves autophagy in healthy people or that chelation improves cancer survival. exposure: Copper exposure, copper-binding mutations and Ctr1 deletion evidence_span: {"source_cache": "artifacts/copper-research/32203415.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f248044309434e00cd35941d0e525a9c73a07e8d78eead20f7d7b6bdcb5f2915", "start_char": 0, "end_char": 1077, "text_sha256": "f248044309434e00cd35941d0e525a9c73a07e8d78eead20f7d7b6bdcb5f2915"} [copper-p32203415] Copper is an essential regulator of the autophagic kinases ULK1/2 to drive lung adenocarcinoma. (2020). https://pubmed.ncbi.nlm.nih.gov/32203415/ DOI: 10.1038/s41556-020-0481-4
    Complete structured claim and evidence

What acts on it

  1. Direct copper interaction supported ULK1 kinase activity in the experimental system.

    Copper → Human unc-51-like autophagy activating kinase ULK1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/copper-research/32203415.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f248044309434e00cd35941d0e525a9c73a07e8d78eead20f7d7b6bdcb5f2915", "start_char": 0, "end_char": 1077, "text_sha256": "f248044309434e00cd35941d0e525a9c73a07e8d78eead20f7d7b6bdcb5f2915"}
    experimental_model
    Recombinant kinase assays, genetic perturbations and lung tumor models
    exposure
    Copper exposure, copper-binding mutations and Ctr1 deletion
    limitations
    Preclinical molecular evidence; not proof that copper supplementation improves autophagy in healthy people or that chelation improves cancer survival.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Human recombinant ULK1/ULK2 with complementary mouse systems
    plain_language
    Copper helps regulate one enzyme that starts cellular recycling.
    primary_references
    [copper-p32203415] Copper is an essential regulator of the autophagic kinases ULK1/2 to drive lung adenocarcinoma. (2020). https://pubmed.ncbi.nlm.nih.gov/32203415/ DOI: 10.1038/s41556-020-0481-4
    tissue_or_cell_type
    Autophagy signaling

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 1235–1246

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant kinase assays, genetic perturbations and lung tumor models · source_derived_draft · unverified_draft

    ### copper-cu-ulk1 Direct copper interaction supported ULK1 kinase activity in the experimental system. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: Copper helps regulate one enzyme that starts cellular recycling. organism: Human recombinant ULK1/ULK2 with complementary mouse systems tissue_or_cell_type: Autophagy signaling experimental_model: Recombinant kinase assays, genetic perturbations and lung tumor models limitations: Preclinical molecular evidence; not proof that copper supplementation improves autophagy in healthy people or that chelation improves cancer survival. exposure: Copper exposure, copper-binding mutations and Ctr1 deletion evidence_span: {"source_cache": "artifacts/copper-research/32203415.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f248044309434e00cd35941d0e525a9c73a07e8d78eead20f7d7b6bdcb5f2915", "start_char": 0, "end_char": 1077, "text_sha256": "f248044309434e00cd35941d0e525a9c73a07e8d78eead20f7d7b6bdcb5f2915"} [copper-p32203415] Copper is an essential regulator of the autophagic kinases ULK1/2 to drive lung adenocarcinoma. (2020). https://pubmed.ncbi.nlm.nih.gov/32203415/ DOI: 10.1038/s41556-020-0481-4
    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