Human insulin-like growth factor 1 receptor / IGF1R

Where it participates (unsigned role)

1. Activation of the cholesterol synthesis pathway but not the synthesis of cholesterol itself is essential for training of myeloid cells, rather the metabolite mevalonate is the mediator of training via activation of IGF1-R and mTOR and subsequent histone modifications in inflammatory pathways, statins which block mevalonate generation prevent trained immunity induction, and monocytes of patients with hyper immunoglobulin D syndrome who are mevalonate kinase deficient and accumulate mevalonate have a constitutive trained immunity phenotype at both immunological and epigenetic levels.

   Mevalonate → Trained immunity, an altered response to a later challenge after the first has ended source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/glucan-research/29328908.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c7d8052926f6be1dad87fedf0023f60ac5441b04f9b8e180c4b1e07edc83eb03", "start_char": 0, "end_char": 1173, "text_sha256": "c7d8052926f6be1dad87fedf0023f60ac5441b04f9b8e180c4b1e07edc83eb03"}

   experimental_model

   Pharmacological and genetic dissection of the cholesterol synthesis pathway, with monocytes from patients accumulating mevalonate

   exposure

   Training of myeloid cells with statins to block mevalonate generation, and monocytes from mevalonate kinase deficient patients

   limitations

   The patient arm is a natural experiment in the opposite direction, which is what makes the mevalonate assignment convincing. The statin result is inhibition of an induced laboratory response.

   nutrient_topic

   Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan

   organism

   Human

   plain_language

   It is the intermediate and not the cholesterol that does the training, and people who cannot clear that intermediate are permanently trained.

   primary_references

   [bg-p29328908] Metabolic Induction of Trained Immunity through the Mevalonate Pathway. (2018). https://pubmed.ncbi.nlm.nih.gov/29328908/ DOI: 10.1016/j.cell.2017.11.025

   tissue_or_cell_type

   Monocyte

   Beta-glucan: a structural family rather than an agent, what decides whether a bound glucan actually signals, the complement route that a cereal and a yeast preparation share, and the unequal human evidence behind each (2026-09-22) · lines 463–474

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Pharmacological and genetic dissection of the cholesterol synthesis pathway, with monocytes from patients accumulating mevalonate · source_derived_draft · unverified_draft

   ### bg-mevalonate-not-cholesterol-trains Activation of the cholesterol synthesis pathway but not the synthesis of cholesterol itself is essential for training of myeloid cells, rather the metabolite mevalonate is the mediator of training via activation of IGF1-R and mTOR and subsequent histone modifications in inflammatory pathways, statins which block mevalonate generation prevent trained immunity induction, and monocytes of patients with hyper immunoglobulin D syndrome who are mevalonate kinase deficient and accumulate mevalonate have a constitutive trained immunity phenotype at both immunological and epigenetic levels. Condition category: normal nutrient_topic: Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. plain_language: It is the intermediate and not the cholesterol that does the training, and people who cannot clear that intermediate are permanently trained. organism: Human tissue_or_cell_type: Monocyte experimental_model: Pharmacological and genetic dissection of the cholesterol synthesis pathway, with monocytes from patients accumulating mevalonate limitations: The patient arm is a natural experiment in the opposite direction, which is what makes the mevalonate assignment convincing. The statin result is inhibition of an induced laboratory response. exposure: Training of myeloid cells with statins to block mevalonate generation, and monocytes from mevalonate kinase deficient patients evidence_span: {"source_cache": "artifacts/glucan-research/29328908.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c7d8052926f6be1dad87fedf0023f60ac5441b04f9b8e180c4b1e07edc83eb03", "start_char": 0, "end_char": 1173, "text_sha256": "c7d8052926f6be1dad87fedf0023f60ac5441b04f9b8e180c4b1e07edc83eb03"} [bg-p29328908] Metabolic Induction of Trained Immunity through the Mevalonate Pathway. (2018). https://pubmed.ncbi.nlm.nih.gov/29328908/ DOI: 10.1016/j.cell.2017.11.025

   Complete structured claim and evidence

2. Lycopene reduced IGF-I-stimulated AP-1 binding capacity in MCF7 cells.

   Lycopene → AP-1 DNA-binding capacity in human MCF7 cells source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/lycopene-research/10798222.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8", "start_char": 0, "end_char": 1731, "text_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8"}

   experimental_model

   Growth-factor stimulation and signaling assays

   exposure

   IGF-I stimulation with lycopene exposure

   limitations

   Cell-line mechanism; not proof of lowered human serum IGF-I or cancer treatment.

   nutrient_topic

   Lycopene research collection; topical membership is not evidence of a direct dietary effect. · Lycopene

   organism

   Human MCF7 breast cancer cells

   plain_language

   A downstream gene-regulatory response also fell.

   primary_references

   [lycopene-p10798222] Lycopene interferes with cell cycle progression and insulin-like growth factor I signaling in mammary cancer cells. (2000). https://pubmed.ncbi.nlm.nih.gov/10798222/ DOI: 10.1207/s15327914nc3601_14

   tissue_or_cell_type

   IRS1 phosphorylation, AP-1 and cell cycle

   Lycopene: absorption, metabolism, nutrient connections and human outcomes (2026-09-17) · lines 676–687

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Growth-factor stimulation and signaling assays · source_derived_draft · unverified_draft

   ### lycopene-ap1 Lycopene reduced IGF-I-stimulated AP-1 binding capacity in MCF7 cells. Condition category: normal nutrient_topic: Lycopene research collection; topical membership is not evidence of a direct dietary effect. plain_language: A downstream gene-regulatory response also fell. organism: Human MCF7 breast cancer cells tissue_or_cell_type: IRS1 phosphorylation, AP-1 and cell cycle experimental_model: Growth-factor stimulation and signaling assays limitations: Cell-line mechanism; not proof of lowered human serum IGF-I or cancer treatment. exposure: IGF-I stimulation with lycopene exposure evidence_span: {"source_cache": "artifacts/lycopene-research/10798222.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8", "start_char": 0, "end_char": 1731, "text_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8"} [lycopene-p10798222] Lycopene interferes with cell cycle progression and insulin-like growth factor I signaling in mammary cancer cells. (2000). https://pubmed.ncbi.nlm.nih.gov/10798222/ DOI: 10.1207/s15327914nc3601_14

   Complete structured claim and evidence

3. Lycopene delayed cell-cycle progression without accompanying apoptotic or necrotic cell death in the tested MCF7 cultures.

   Lycopene → MCF7 breast cancer cell cycle progression source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/lycopene-research/10798222.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8", "start_char": 0, "end_char": 1731, "text_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8"}

   experimental_model

   Growth-factor stimulation and signaling assays

   exposure

   IGF-I stimulation with lycopene exposure

   limitations

   Cell-line mechanism; not proof of lowered human serum IGF-I or cancer treatment.

   nutrient_topic

   Lycopene research collection; topical membership is not evidence of a direct dietary effect. · Lycopene

   organism

   Human MCF7 breast cancer cells

   plain_language

   Slower growth was distinguished from simply killing the cells.

   primary_references

   [lycopene-p10798222] Lycopene interferes with cell cycle progression and insulin-like growth factor I signaling in mammary cancer cells. (2000). https://pubmed.ncbi.nlm.nih.gov/10798222/ DOI: 10.1207/s15327914nc3601_14

   tissue_or_cell_type

   IRS1 phosphorylation, AP-1 and cell cycle

   Lycopene: absorption, metabolism, nutrient connections and human outcomes (2026-09-17) · lines 702–713

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Growth-factor stimulation and signaling assays · source_derived_draft · unverified_draft

   ### lycopene-cell-cycle Lycopene delayed cell-cycle progression without accompanying apoptotic or necrotic cell death in the tested MCF7 cultures. Condition category: normal nutrient_topic: Lycopene research collection; topical membership is not evidence of a direct dietary effect. plain_language: Slower growth was distinguished from simply killing the cells. organism: Human MCF7 breast cancer cells tissue_or_cell_type: IRS1 phosphorylation, AP-1 and cell cycle experimental_model: Growth-factor stimulation and signaling assays limitations: Cell-line mechanism; not proof of lowered human serum IGF-I or cancer treatment. exposure: IGF-I stimulation with lycopene exposure evidence_span: {"source_cache": "artifacts/lycopene-research/10798222.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8", "start_char": 0, "end_char": 1731, "text_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8"} [lycopene-p10798222] Lycopene interferes with cell cycle progression and insulin-like growth factor I signaling in mammary cancer cells. (2000). https://pubmed.ncbi.nlm.nih.gov/10798222/ DOI: 10.1207/s15327914nc3601_14

   Complete structured claim and evidence

4. Lycopene increased membrane-associated IGF-binding proteins without changing IGF-I receptor number or affinity.

   Lycopene → Membrane-associated IGF-binding proteins in MCF7 cells source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/lycopene-research/10798222.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8", "start_char": 0, "end_char": 1731, "text_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8"}

   experimental_model

   Growth-factor stimulation and signaling assays

   exposure

   IGF-I stimulation with lycopene exposure

   limitations

   Cell-line mechanism; not proof of lowered human serum IGF-I or cancer treatment.

   nutrient_topic

   Lycopene research collection; topical membership is not evidence of a direct dietary effect. · Lycopene

   organism

   Human MCF7 breast cancer cells

   plain_language

   The experiment points to altered signal regulation rather than fewer receptors.

   primary_references

   [lycopene-p10798222] Lycopene interferes with cell cycle progression and insulin-like growth factor I signaling in mammary cancer cells. (2000). https://pubmed.ncbi.nlm.nih.gov/10798222/ DOI: 10.1207/s15327914nc3601_14

   tissue_or_cell_type

   IRS1 phosphorylation, AP-1 and cell cycle

   Lycopene: absorption, metabolism, nutrient connections and human outcomes (2026-09-17) · lines 689–700

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Growth-factor stimulation and signaling assays · source_derived_draft · unverified_draft

   ### lycopene-igfbp Lycopene increased membrane-associated IGF-binding proteins without changing IGF-I receptor number or affinity. Condition category: normal nutrient_topic: Lycopene research collection; topical membership is not evidence of a direct dietary effect. plain_language: The experiment points to altered signal regulation rather than fewer receptors. organism: Human MCF7 breast cancer cells tissue_or_cell_type: IRS1 phosphorylation, AP-1 and cell cycle experimental_model: Growth-factor stimulation and signaling assays limitations: Cell-line mechanism; not proof of lowered human serum IGF-I or cancer treatment. exposure: IGF-I stimulation with lycopene exposure evidence_span: {"source_cache": "artifacts/lycopene-research/10798222.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8", "start_char": 0, "end_char": 1731, "text_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8"} [lycopene-p10798222] Lycopene interferes with cell cycle progression and insulin-like growth factor I signaling in mammary cancer cells. (2000). https://pubmed.ncbi.nlm.nih.gov/10798222/ DOI: 10.1207/s15327914nc3601_14

   Complete structured claim and evidence

5. Lycopene reduced IGF-I-stimulated IRS1 tyrosine phosphorylation in MCF7 cells.

   Lycopene → IRS1 tyrosine phosphorylation in human MCF7 cells source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/lycopene-research/10798222.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8", "start_char": 0, "end_char": 1731, "text_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8"}

   experimental_model

   Growth-factor stimulation and signaling assays

   exposure

   IGF-I stimulation with lycopene exposure

   limitations

   Cell-line mechanism; not proof of lowered human serum IGF-I or cancer treatment.

   nutrient_topic

   Lycopene research collection; topical membership is not evidence of a direct dietary effect. · Lycopene

   organism

   Human MCF7 breast cancer cells

   plain_language

   The growth signal was weaker at an intracellular relay.

   primary_references

   [lycopene-p10798222] Lycopene interferes with cell cycle progression and insulin-like growth factor I signaling in mammary cancer cells. (2000). https://pubmed.ncbi.nlm.nih.gov/10798222/ DOI: 10.1207/s15327914nc3601_14

   tissue_or_cell_type

   IRS1 phosphorylation, AP-1 and cell cycle

   Lycopene: absorption, metabolism, nutrient connections and human outcomes (2026-09-17) · lines 663–674

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Growth-factor stimulation and signaling assays · source_derived_draft · unverified_draft

   ### lycopene-irs1 Lycopene reduced IGF-I-stimulated IRS1 tyrosine phosphorylation in MCF7 cells. Condition category: normal nutrient_topic: Lycopene research collection; topical membership is not evidence of a direct dietary effect. plain_language: The growth signal was weaker at an intracellular relay. organism: Human MCF7 breast cancer cells tissue_or_cell_type: IRS1 phosphorylation, AP-1 and cell cycle experimental_model: Growth-factor stimulation and signaling assays limitations: Cell-line mechanism; not proof of lowered human serum IGF-I or cancer treatment. exposure: IGF-I stimulation with lycopene exposure evidence_span: {"source_cache": "artifacts/lycopene-research/10798222.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8", "start_char": 0, "end_char": 1731, "text_sha256": "f9229468bbed86c3c4fdbb24f80d139f5cac41e1692195090d19a195bcd144e8"} [lycopene-p10798222] Lycopene interferes with cell cycle progression and insulin-like growth factor I signaling in mammary cancer cells. (2000). https://pubmed.ncbi.nlm.nih.gov/10798222/ DOI: 10.1207/s15327914nc3601_14

   Complete structured claim and evidence